Search Images Maps Play YouTube News Gmail Drive More »
Sign in
Screen reader users: click this link for accessible mode. Accessible mode has the same essential features but works better with your reader.

Patents

  1. Advanced Patent Search
Publication numberUS20060174884 A1
Publication typeApplication
Application numberUS 11/386,807
Publication dateAug 10, 2006
Filing dateMar 23, 2006
Priority dateJun 21, 2001
Also published asUS7246618, US8573205, US20030111078, US20080072901
Publication number11386807, 386807, US 2006/0174884 A1, US 2006/174884 A1, US 20060174884 A1, US 20060174884A1, US 2006174884 A1, US 2006174884A1, US-A1-20060174884, US-A1-2006174884, US2006/0174884A1, US2006/174884A1, US20060174884 A1, US20060174884A1, US2006174884 A1, US2006174884A1
InventorsNader Habashi
Original AssigneeHabashi Nader M
Export CitationBiBTeX, EndNote, RefMan
External Links: USPTO, USPTO Assignment, Espacenet
Ventilation method and control of a ventilator based on same
US 20060174884 A1
Abstract
The invention provides an improved ventilation method and method for controlling a ventilator apparatus in accordance with same. More specifically, the present invention relates to a method of controlling a ventilator apparatus comprising the steps of placing a ventilator in a mode capable of adjusting airway pressure (P) and time (T), monitoring expiratory gas flow, analyzing the expiratory gas flow over time (T) to establish an expiratory gas flow pattern, and setting and/or adjusting a low time (T2) based on the expiratory gas flow pattern. Alternatively, the present invention relates to a method of controlling a ventilator apparatus comprising the steps of placing a ventilator in a mode capable of adjusting airway pressure (P) and time (T), and setting a low airway pressure (P2) of substantially zero cmH2O.
Images(9)
Previous page
Next page
Claims(9)
1-14. (canceled)
15. A method of weaning from ventilation comprising the step of substantially contemporaneously adjusting a high airway pressure (P1) and a high time (T1).
16. The method of claim 15, wherein the adjusting step comprises decreasing P1 and increasing T1.
17. The method of claim 16, wherein P1 is decreased at a rate of about 2 cmH2O per hour and T1 is increased by about 0.5 to 1.0 s substantially contemporaneously with each decrease in P1.
18. The method of claim 16, wherein P1 is decreased in increments of about 4 cmH2O and T1 is increased in increments of about 2 s.
19. The method of claim 16, further comprising the step of transitioning ventilation from a preset continuous positive airway pressure (CPAP) level mode with an intermittent release to a substantially continuous positive airway pressure (CPAP) mode.
20. The method of claim 16, further comprising the step of transitioning ventilation from a preset continuous positive airway pressure (CPAP) level mode with an intermittent release to a substantially continuous positive airway pressure (CPAP) mode with automatic tube compensation (ATC).
21. The method of claim 19, further comprising the steps of:
a) monitoring blood oxygen levels,
b) monitoring blood carbon dioxide levels,
c) determining the ratio of spontaneous minute ventilation to machine minute ventilation, and
d) determining the level of sedation.
22. The method of claim 19, further comprising the steps of substantially simultaneously decreasing machine minute ventilation and increasing spontaneous minute ventilation to transition from the CPAP mode to an unassisted breathing mode.
Description
CROSS-REFERENCE TO RELATED APPLICATIONS

This application is a divisional of U.S. application Ser. No. 10/176,710 filed Jun. 20, 2002, which claims priority to U.S. Provisional Application No. 60/299,928 filed Jun. 21, 2001.

FIELD OF THE INVENTION

The invention related to the field of ventilating human patients. More particularly, the present invention relates to an improved method of initiation, management and/or weaning of airway pressure release ventilation and for controlling a ventilator in accordance with same.

BACKGROUND OF THE INVENTION

Airway pressure release ventilation (APRV) is a mode of ventilation believed to offer advantages as a lung protective ventilator strategy. APRV is a form of continuous positive airway pressure (CPAP) with an intermittent release phase from a preset CPAP level.

During APRV, ventilation occurs on the expiratory limb. The resultant expiratory tidal volume decreases lung volume, eliminating the need to elevate end inspiratory pressure above the upper inflection point. Therefore, tidal volume reduction is unnecessary. CPAP levels can be set with the goal of optimizing recruitment without increasing the potential for over distension. Consequently, end inspiratory pressure can be limited despite more complete recruitment and ventilation can be maintained.

APRV is also associated with reduction or elimination of sedative, inotropic and neuromuscular blocking agents.

APRV is a form of positive pressure ventilation that augments alveolar ventilation and lowers peak airway pressure. Published data on APRV has documented airway pressure reduction on the order of 30 to 75 percent over conventional volume and pressure cycled ventilation during experimental and clinical studies. Such reduction of airway pressure may reduce the risk of VILI. APRV improves ventilation to perfusion ratio (VA/Q) matching and reduces shunt fraction compared to conventional ventilation. Studies performed utilizing multiple inert gas dilution and excretion technique (MIGET) have demonstrated less shunt fraction, and dead space ventilation. Such studies suggest that APRV is associated with more uniform distribution inspired gas and less dead space ventilation than conventional positive pressure ventilation.

APRV has been associated with improved hemodynamics. In a 10-year review of APRV, Calzia reported no adverse hemodynamic effects. Several studies have documented improved cardiac output, blood pressure and oxygen delivery. Consideration of APRV as an alternative to pharmacological or fluid therapy in the hemodynamically-compromised, mechanically-ventilated patient has been recommended in several case reports.

However, most patients with ALI/ARDS exhibit expiratory flow limitations. Expiratory flow limitations results in dynamic hyperinflation and intrinsic positive end expiratory pressure (PEEP) development. In addition, ARDS patients experience increased flow resistance from external ventilator valving and gas flow path circuitry including the endotracheal tube and the external application of PEEP.

Several mechanisms can induce expiratory flow limitations in ALI/ARDS. In ALI/ARDS both FRC and expiratory flow reserve is reduced. Pulmonary edema development and superimposed pressure result in increased airway closing volume and trapped volume. In addition, the reduced number of functional lung units (de-recruited lung units and enhanced airway closure) decrease expiratory flow reserve further. Low volume ventilation promotes small airway closure and gas trapping. In addition elevated levels of PEEP increase expiratory flow resistance. In addition to downstream resistance, maximal expiratory flow depends on lung volume. The elastic recoil pressure stored in the proceeding lung inflation determines the rate of passive lung deflation.

APRV expiratory flow is enhanced by utilization of an open breathing system and use of low (0-5 cmH2O) end expiratory pressure. EELV is maintained by limiting the release time and titrated to the inflection point of the flow volume curve.

PSV required significant increases in pressure support levels (airway pressure) to match the same minute ventilation.

Conventional lung protective strategies are associated with increased use of sedative agents and neuromuscular blocking agents (NMBA).

In addition to drug cost reduction, elimination of NMBA is thought to reduce the likelihood of associated complications such as prolonged paralysis and may facilitate weaning from mechanical ventilation.

Mechanical ventilation remains the mainstay management for acute respiratory failure. In contrast, shear force stress from repetitive airway closure during the tidal cycle from mechanical ventilation results in low volume lung injury.

End expiratory lung volume was maintained by setting PEEP levels to 2 cmH2O above the lower inflection point.

Such important differences between these studies limited conclusions as to the effectiveness of low tidal ventilation limiting ventilator associated lung injury (VALI).

Recent completion of the large controlled randomized ARDSNet trial documented improved survival and ventilator free days utilizing low tidal volume ventilation (6 ml/kg) vs. traditional tidal volume ventilation (12 ml/kg). although the low tidal volume group (6 ml/kg) and traditional tidal volume group (12 ml/kg) groups utilized identical PEEP/FiO2 scales, PEEP levels were significantly higher in the low tidal volume group. Higher PEEP levels were required in the low tidal volume group in order to meet oxygenation goals of the study. Despite improved survival in the low tidal volume group (6 ml/kg) over traditional tidal volume group (12 ml/kg), survival was higher in the Amato study. The ARDSNet trial also failed to demonstrate any difference in the incidence of barotraumas. The higher PEEP requirements and the potential for significant intrinsic PEEP from higher respiratory frequency in the lower tidal volume group, may have obscured potential contribution of elevated end expiratory pressure on survival. Further studies are contemplated to address the issue of elevated end expiratory pressure.

In the prior art, utilization of the quasi-static inspiratory pressure versus volume (P-V) curve has been advocated as the basis for controlling a ventilator to carry out mechanical ventilation.

SUMMARY OF THE INVENTION

The P-V curve represents the entire respiratory system and may not adequately reflect the individual air spaces.

The invention further recognizes that recruitment continues above the inflection point and may continue at airway pressures beyond 30 cmH2O and that the primary mechanism of lung volume change may be recruitment/de-recruitment (R/D) rather than isotropic and anisotropic alveolar volume change. Lung volume change to 80% of total lung capacity (TLC) may well be a result of alveolar number increase (RID) rather than alveolar size. Furthermore, recruitment is an end inspiratory phenomenon and may be more closely related to plateau pressure rather than PEEP. Therefore, to prevent tidal recruitment/de-recruitment (RID), cyclic shear stress and low volume lung injury, the invention contemplates that higher pressure may be required to achieve complete recruitment. It is recognized that if PEEP levels are set to end inspiratory pressure in order to completely recruit the lung, the superimposition of tidal ventilation could result in over-distension and high volume lung injury despite tidal volume reduction.

Accordingly, the invention recognizes that recruitment is an inflation phenomenon which continues beyond conventional PEEP levels. Recruitment requires enough pressure to overcome threshold-opening pressures and the superimposed pressure of the airspace. Plateau pressure or continuous positive airway pressure (CPAP) rather than PEEP level may be more appropriate determinants of full lung recruitment. PEEP conceptually prevents de-recruitment after a sustained inflation. Airway closure or de-recruitment is a deflation phenomenon. Therefore, in accordance with the invention, PEEP may be more suitable set to the inflection point of the deflation limb of the P-V curve rather than that of the inflation limb.

Greater hysteresis results from a downward and right displacement of the inflation limb of the P-V curve.

Rather than PEEP, plateau or CPAP levels should be utilized for bringing about airway opening (recruitment), allowing substantially complete recruitment. In addition to adequate threshold pressure, complete recruitment requires constant inflation in order to sustain recruitment. Furthermore, sustained recruitment facilitates ventilation on the deflation limb. Ventilation occurs on the deflation limb of the P-V curve only after a sustained recruitment maneuver. Sustained inflation pushes the P-V curve to the outer envelope on to the deflation limb. Stress relaxation accounts for a pressure reduction on the order of 20% within the initial 4 seconds of inflation.

In accordance with the invention, APRV mode ventilation is established based on an initial set of ventilation parameters selected as described in further detail below. Once ventilation has been initiated, the parameter, T2, which defines the duration of the ventilator release phase, is monitored and adjusted according to at least one and preferable several alternative methods.

One method is to measure the expiratory gas flow rate during expiration and to adjust T2, if necessary, such that T2 is terminated when the rate of expiratory gas flow is at a value of about 25% to 50% of its absolute peak value during expiration. To achieve this, the ventilator is controlled to monitor the expiratory gas flow rate and terminate the release phase when the flow rate reaches a value within the aforementioned range.

Another method is to monitor expiratory flow and determine, based on the flow pattern, whether the flow is of a restrictive or obstructive nature, and adjust T2 accordingly. According to yet another method, the expiratory flow is monitored for the presence of an inflection point and T2 is adjusted as required to substantially eliminate or at least reduce the inflection point.

In the event of hypercarbia, the highest airway pressure achieved during inspiration (P1) and the duration of the positive pressure phase (T1) are both incrementally increased substantially contemporaneously once or more as needed until blood carbon dioxide declines to an acceptable level.

Accordingly to yet another aspect of the invention, weaning from ventilation is carried out by initiating a series of successive reductions in P1, each of which is accompanied by a substantially contemporaneous, increase in the duration of inspiration T1 such that over time, ventilation is transitioned from APRV to a substantially CPAP mode.

Applicant's ventilation method and method for controlling a ventilation apparatus based on same provides significant advantages over the prior art. These advantages include an increase in vent free days, lower ventilator-related drug costs, reduced ventilator associated complications, reduced likelihood of high volume lung injury, and reduced likelihood of low volume lung injury. These and other objects and advantages of the invention will become more apparent to a person of ordinary skill in the art in light of the following detailed description and appended drawings.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a flowchart illustrating a preferred embodiment of a ventilation method and control of a ventilator based on same according to the invention;

FIG. 2 is a schematic airway pressure versus time tracing for airway pressure release ventilation;

FIG. 3 is a airway pressure versus time tracing during the inspiratory (P1) phase of ventilation;

FIG. 4 is an airway volume versus pressure curve illustrating a shift from the inspiratory limb to the expiratory limb thereof;

FIG. 5 is an inspiratory and expiratory gas flow versus time tracing for airway pressure release ventilation;

FIG. 6 is an expiratory gas flow versus time tracing;

FIG. 7 is a set of expiratory gas flow versus time tracing illustrating determination of whether flow pattern is normal, restrictive or obstructive based on the shape of the tracing, and

FIG. 8 is a set of airway pressure versus time tracings illustrating ventilation weaning by successive reductions in pressure PI and substantially contemporaneous increases in time T1.

DETAILED DESCRIPTION

An operator interface coupled to the control unit typically includes a graphical user interface as well as a keyboard and/or pointing device to enable an operator to select the operating mode of the ventilator and/or to enter or edit patient data and operating parameters such as the pressures, times, flows, and/or volumes associated with one or more ventilation cycles.

Referring to FIG. 1, the invention contemplates initiating ventilation of a patient in an APRV mode based on initial oxygenation and ventilation settings. The airway pressure during expiration (P2) is substantially zero throughout ventilation to allow for the rapid acceleration of expiratory gas flow rates. Typically, the fraction of oxygen in the inspired gas (FiO2) is initially set at about 0.5 to 1.0 (i.e. about 50% to 100%). The highest airway pressure achieved during inspiration (PI) must be sufficiently high to overcome airspace closing forces and initiate recruitment of lung volume. PI may suitably be initialized at a default value of about 35 cmH2O. Alternatively, PI may be established based either on the severity and type of lung injury or based on recruitment pressure requirements. The latter method is preferred in cases where the ventilation/perfusion ratio is less than or equal to about two hundred millimeters of mercury (200 mmHg). The ventilation perfusion ratio is preferably monitored continuously. It is the ratio of the partial pressure of oxygen in the blood of the patient to the fraction of oxygen present in the inspired gas (i.e. PaO2/FiO2 but is commonly abbreviated as P/F).

Where the type and severity of lung injury are characterized by a P/F of greater than about 350 mmHg, an initial value of P1 within the range of about 20 cmH2O to 28 cmH2O is preferably established. On the other hand, if the P/F ratio is less than about 350 mmHg, P1 is preferably initialized within the range of about 28 cmH2O to 35 cmH2O.

In situations where the P/F ration is less than or equal to about 200 mm Hg, such as may occur where the patient's initial injury is non-pulmonary and/or lung injury is of an indirect nature, the invention contemplates establishment of P1 at a value of between about 35 mmHg and 40 mmHg but preferably not appreciably above 40 mmHg.

Initially, the duration of the positive pressure phase (Ti) is established at a value within the range of about 5.0 to about 6.0 seconds unless the measured PaCO2 is greater than about 60 mmHg.

Once initial values of P1, P2, T1 and T2 have been established, ventilation continues in a repetitive APRV mode cycle generally as illustrated in FIG. 2. During management of ventilation in accordance with the invention, the initial values of one or more of these parameters are re-assessed and modified in accordance with measured parameters as will now be described with continued reference to FIG. 1.

In management of ventilation in accordance with the invention, a principal goal is to maintain the level of carbon dioxide in the blood of the ventilated patient (PaCo2) at a level of less than or equal to about 50 mmHg. Toward that end, arterial PaCO2 is monitored continuously or measured as clinically indicated and the ventilator controlled to adjust ventilation as follows. Any time after ventilation has commenced, but preferably soon thereafter or promptly upon any indication of hypercarbia (PaCO2 above about 50 mmHg), the setting of T2 is optionally but preferably checked and re-adjusted if necessary. According to the invention, optimal end expiratory lung volume is maintained by titration of the duration of the expiration or release phase by terminating T2 based on expiratory gas flow. To do so, the flow rate of the expiratory gas is measured by the ventilator and checked in relation to the time at which the controller of the ventilator initiates termination of the release phase. The expiratory exhaust valve should be actuated to terminate the release phase T2, at a time when the flow rate of the expiratory gas has decreased to about 25% to 50% of its absolute peak expiratory flow rate (PEFR). An example is illustrated in FIG. 5. In that example, T2 (sometimes referred to as Tlow) terminates by controlling the expiratory exhaust valve to terminate the release phase when the expiratory gas flow rate diminishes to 40% PEFR.

If monitoring of PaCO2 indicates hypocarbia is present (i.e. PaCO2 less than about 50 mmHg), T1 is increased by about 0.5 seconds while maintaining PI substantially unchanged. Should the patient remain hypocarbic as indicated by subsequent measure of PaCO2, weaning in the manner to be described may be initiated provided oxygenation is satisfactory and weaning is not otherwise contraindicated based on criteria to be described further below.

The hypercarbic patient though is not to be weaned. In the event of hypercarbia, the invention contemplates assessment of the expiratory flow pattern before making significant further adjustments to ventilation parameters. This assessment can readily be carried out by a software program stored within the control unit of the ventilator which carries out automated analysis of the expiration flow versus time tracing. As illustrated in FIG. 7, normal expiratory flow is characterized by flow which declines substantially monotonically from the onset of the release phase through its termination and does not fall off prematurely or abruptly. Restrictive flow in contrast declines rapidly from the onset of the release phase to zero or a relatively small value. Obstructive flow tends to be more extended in duration and is characterized by an inflection point beyond which the rate of flow falls off markedly from its initial rate. FIG. 6 illustrates another example of an obstructive flow pattern. Based on analysis of flow data provided by expiratory flow sensors, the control unit of the ventilator is programmed to determine whether flow is obstructive or restrictive based on the characteristics just described. If it is determined that obstructive or restrictive flow is present, the invention contemplates adjusting T2 before making any other significant adjustments to ventilation parameters. This can be done according to either of two alternative methods.

One method is to adjust T2 to a predetermined value according to whether flow is either obstructive or restrictive but allowing T2 to remain at its previous value if flow is normal. In the case of restrictive flow, T2 should be adjusted to less than about 0.7 seconds. On the other hand, obstructive flow calls for a T2 of greater duration, preferably greater than about 0.7 seconds with 1.0 to 1.2 being typical.

PaCO2 should then be reassessed and concomitant increases of about 0.5 seconds in T1 and about 2 cmH2O in P1 repeated as indicated in FIG. 1 until the patient is no longer hypercarbic.

Upon meeting the latter objective, weaning in the manner to be described may be initiated provided the ventilation goal described earlier (i.e. a PaCO2 of less than about 50 mmHg) is met and weaning is not otherwise contraindicated.

If such action does not result in raising oxygenation and saturation to at least the goals of about PaO2 of about 80 mmHg and SaO2 of about 95%, P1 is increased to a maximum of about 45 cmH2O and Ti is progressively further increased by about 0.5 seconds to 1.0 seconds.

Once those oxygenation and saturation goals are met, ventilation is controlled to maintain those goals while progressively decreasing FiO2 and P1 toward the levels at which initiation of weaning can be considered. More particularly, P1 is decreased by about 1 cmH2O per hour while FiO2 is decreased by about 0.05 about every thirty (30) minutes while maintaining an oxygen saturation of at least about 95%.

That is, when PaCO2 remains below about 50 mmHg and SaO2 remains at least about 95% at a P1 of about 35 cmH2O and FiO2, if previously higher, has been weaned to a level of not greater than about 0.5

However, during the second stage, the reductions in P1 take place in increments of about 4 cmH2O and the increases in T1 are each about 2.0 seconds.

Once the patient is tolerating CPAP at about 5 cmH2O with FiO2 of not greater than about 0.5, the patient's ability to maintain unassisted breathing is assessed, preferably for at least about 2 hours or more.

a.) SPO2 of at least about 0.90 and/or PaO2 of at least about 60 mmHg;

b.) tidal volume of not less than about 4 ml/kg of ideal bodyweight;

c.) respiration rate not significantly above about 35 breaths per minute; and

d.) lack of respiratory distress, with such distress being indicated by the presence of any two or more of the following:

    • i) Heart rate greater than 120% of the 0600-hour rate (through less than about 5 minutes above such rate may be considered acceptable)
    • ii) marked use of accessory muscles to assist breathing;
    • iii) thoroco-abdominal paradox;
    • iv) diaphoresis and/or
    • v) marked subjected dyspnea.

If there is an indication of respiratory distress, CPAP at an airway pressure of about 10 cmH2O should be resumed and monitoring and reassessment carried out as needed. However, if criteria a) through d) above are all satisfied, the patient may be transitioned to substantially unassisted breathing such as by extubation with face mask, nasal prong oxygen or room air, T-tube breathing, tracheotomy mask breathing or use of high flow CPAP at about 5 cmH2O.

During all phases of ventilation including initiation, management and weaning, the patent should be reassessed at least about every two hours and more frequently if indicated. Blood gas measurements (PaO2 and SaO2 and PCO2) on which govern control of ventilation according to the invention should be monitored not less frequently than every two hours though substantially continuous monitoring of all parameters would be considered ideal. Blood gas measurements (PaO2 and SaO2 and PaCO2) that govern control of ventilation according to the invention should be monitored not less frequently than every two hours though substantially continuous monitoring of all parameters would be considered ideal.

Just prior to and during weaning at least one special assessment should be conducted daily, preferably between 0600 and 1000 hours. If not possible to do so, a delay of not more than about four hours could be tolerated. Weaning should not be initiated or continued further unless:

a) at least about 12 hours have passed since initial ventilation settings were established or first changed,

b) the patient is not receiving neuromuscular blocking agents and is without neuromuscular blockade, and

c) Systolic arterial pressure is at least about 90 mmHg without vasopressors (other than “renal” dose dopamine).

If these criteria are all met, a trial should be conducted by ventilating the patent in CPAP mode at about 5 cmH2O and an FiO2 of about 0.5 for about five (5) minutes. If the respiration rate of the patient does not exceed about 35 breaths per minute (bpm) during the five (5) minute period weaning as described above may proceed. However, if during the five (5) minute period the respiration rate exceeds about 35 bpm it should be determined whether such tachypnea is associated with anxiety. If so, administer appropriate treatment for the anxiety and repeat the trial within about four (4) hours. If tachypnea does not appear to be associated with anxiety, resume management of ventilation at the parameter settings in effect prior to the trial and resume management of ventilation as described above. Re-assess at least daily until weaning as described above can be initiated.

Non-Patent Citations
Reference
1 *Esteban et al., A Comparison of Four Methods of Weaning Patients From Mechanical Ventilation, 2/9/95, Massachusetts Medical Society, The New England Journal of Medicine Vol. 332 pages 345-350
Referenced by
Citing PatentFiling datePublication dateApplicantTitle
US8695597 *Jun 2, 2008Apr 15, 2014Dräger Medical GmbHProcess for operating a respirator and/or anesthesia device in the APRV mode with the %PEF criterion and a device operated correspondingly
US20080295840 *Jun 2, 2008Dec 4, 2008Drager Medical Ag & Co. KgProcess for operating a respirator and/or anesthesia device in the aprv mode with the %pef criterion and a device operated correspondingly
US20090205663 *Feb 6, 2009Aug 20, 2009Nellcor Puritan Bennett LlcConfiguring the operation of an alternating pressure ventilation mode
DE102007026035B3 *Jun 4, 2007Mar 27, 2008Dräger Medical AG & Co. KGOperating breathing and/or anaesthetizing apparatus in APRV mode involves detecting spontaneous expiration effort, initiating pressure release phase if detected spontaneous expiration effort occurs in predefined trigger window
DE102007026036B3 *Jun 4, 2007Mar 27, 2008Dräger Medical AG & Co. KGOperation of a respiratory and/or anesthetic system matches the actual and set portion of the peak expiratory flow
DE102007052472A1Nov 2, 2007May 14, 2009Dräger Medical AG & Co. KGVerfahren zum Betreiben einer Beatmungs- und/oder Anästhesievorrichtung im APRV-Modus unter Berücksichtigung der Impedanz und/oder der Impedanzänderung
Classifications
U.S. Classification128/204.21, 128/204.18, 128/200.24, 128/203.12, 128/204.23
International ClassificationA61M16/00, A62B7/00
Cooperative ClassificationA61M2016/0039, A61M2205/3331, A61M2230/205, A61M2016/0042, A61M16/00, A61M2230/202
European ClassificationA61M16/00
Legal Events
DateCodeEventDescription
Jul 8, 2010ASAssignment
Owner name: INTENSIVE CARE ON-LINE NETWORK, INC.,MARYLAND
Free format text: ASSIGNMENT OF ASSIGNORS INTEREST;ASSIGNOR:HABASHI, NADER M.;REEL/FRAME:24651/457
Effective date: 20100708
Owner name: INTENSIVE CARE ON-LINE NETWORK, INC., MARYLAND
Free format text: ASSIGNMENT OF ASSIGNORS INTEREST;ASSIGNOR:HABASHI, NADER M.;REEL/FRAME:024651/0457