An effective treatment can be a multiple daily mechanical lung recruitment protocol that serves to mobilize and transport the retained endobronchial secretions from the peripheral airways up through the conducting airways to be expectorated.
During IPV® lung recruitment, a Newtonian pumping action (for each action there is an equal and opposite reaction) serves to mobilize and raise the retained endobronchial secretions by first reducing the cohesive and adhesive forces with a topical aerosol, and then raising the retained endobronchial secretions by employing an air distal (behind) to the mobilized endobronchial secretions.
The unique percussive intrapulmonary counter flow technology provides for a progressive therapeutic lung recruitment, while maintaining a lung protective strategy.
A recent PEER review discussed the components of the mucus protein and polysaccharides relative to possible airway recruitment when, in reality, a breakdown of the constituents of the primary secretions is of little concern in mechanically mobilizing and raising the retained endobronchial secretions. It is the viscosity of the mucus, and the ability of the therapeutic protocol to mobilize and mechanically raise the retained endobronchial secretions that is of primary therapeutic consideration. Therefore, a clinical protocol that addresses the daily mobilization and the raising of retained peripheral endobronchial secretions may be the most effective means of decreasing the severity of the acute endobronchial infections associated with cystic fibrosis.
Manual chest physiotherapy has long been an effective means of recruiting retained endobronchial secretions in the hospitalized patient with an acute infection. Some years ago, a pulsating (squeezing) vest was designed to mimic manual chest physiotherapy. While the fitting of the Vest has advanced in design, the primary restrictions of the protocol remain. Essentially, the vest remains an upper airway secretion clearance device.
The vest does not recruit peripheral bronchioles with mucosal and submucosal edema obstructions, nor does it produce an all-important enhanced peripheral “Circulatory Vesicular Peristalsis” within the intrathoracic vesicular circulations.
Currently, within the United States, it is calculated that there may be well over 20,000,000 moderate to severe emphysematous patients as well as many more patients with other pulmonary considerations who employ their own OTC therapy because ethical medicine has not provided them with what they may have perceived as being clinically effective.
We as mortals are blessed with an initial cardiopulmonary reserve of some 80%. Childhood bronchitis is typically demonstrated in the child who starts in the fall with a non-productive cough which may be present until late spring. The cough is often treated with cough drops and syrups. This scenario becomes a normal winter ritual accepted by other family members.
When the persistent low-grade pulmonary infection of bronchitis is insulted by a common cold or other compromise, the patient can become clinically decompensated by a severe pulmonary infection characterized by a slow recovery. As the years progress, each acute insult to the existing bronchitis encroaches upon the patient’s pulmonary reserve, leading to Chronic Bronchitis. All too often the patient may become a smoker, which accelerates the onset of chronicity. Some become “couch potatoes,” leading to obesity.
Each pulmonary infection reduces the patient’s cardiopulmonary reserves. Finally, the chronic bronchitis patient enters the hospital with a major endobronchial infection.
After arriving back home with an obvious labored breathing, using a bronchodilator inhaler, etc., the patient’s friends ask the patient, “What happened to you?” The patient’s reply may be. “I JUST GOT EMPHYSEMA”.
The fact is, the patient had a possible congenital pre-disposition to bronchitis, which, over many years, became chronic, with an insidious loss of cardiopulmonary reserve. This loss of reserve progressed to the point where the bronchial blood supply to the pulmonary structures had been impaired long enough to produce a chronic (without remission) bronchial blood flow ischemia followed by necrotic encroachment upon the Bronchiolar blood supply. Thus, pulmonary emphysema may be described as an ischemic end stage lung disease.
Interestingly, some years ago some clinicians were asked if they would rather be born with congenital asthma or a congenital bronchitis. Some stated congenital bronchitis. The fact is, the asthmatic patient rarely becomes emphysematous, if at all, while the bronchitis patient almost always ultimately develops pulmonary emphysema.
The reason for this is that the asthmatic is free of alveolar hyperinflation secondary to chronic peripheral airway obstruction the majority of time. While the patient with chronic bronchitis develops an unrelenting chronic alveolar hyperinflation secondary to bronchial airway secretion retention and pre-alveoli mucosal and sub mucosal edema, leading to bronchial blood flow encroachment within the bronchial circulations.
The average clinician may understand perfusion of the major intrathoracic pulmonary circulation while the minor CRITICAL “Intrathoracic Bronchial Circulation” may not be therapeutically addressed.
THE PULMONARY CIRCULATION BY NETTER COURTESY OF CIBA® 1976
Guyton, in his textbook on “Medical Physiology” describes the bronchial and lymph circulation as follows:
“THE BRONCHIAL VESSELS: A minor accessory arterial blood supply to the lungs exits directly from the aorta through usually one bronchial artery to the right lung and two bronchial arteries to the left lung.
The blood flowing in the bronchial arteries is oxygenated by “arterial” blood, and it supplies the supporting tissues of the lungs, including the connective tissue, the septa, and the large and small bronchi.
After this bronchial arterial blood has passed through the supporting tissues, it empties into the pulmonary arteries and veins and enters the left atrium rather than passing back to the right atrium. Therefore an average of about 1 percent (but on rare occasions as high as 10 to 50 per cent) more blood flows through the left side of the heart than through the right side.
THE LYMPHATICS: Lymphatics extend from all the supportive tissues of the lung to the hilus pulmonis and thence into the thoracic duct. Particulate matter entering the alveoli is usually removed very rapidly via these channels, and protein is also removed from the lung tissues, thereby preventing edema.”
With a primary understanding of the transition from Bronchitis to chronic Bronchitis to Emphysema, does it not make more sense to prophylactically start a therapeutic regime directed toward limiting the progression of the disease process? This would have to be accomplished by an educational alliance between the patient and the patho-physiological knowledgeable clinician.
By applying oversimplified logic, would it not be advisable to project a therapeutic regime on a daily basis that therapeutically recruits the peripheral lung by resolving processes that create mucosal and submucosal edema within the terminal bronchial airways?
The average patient with COPD is usually seen by their physician only during their hospitalization, which is generally resultant from an acute pulmonary infection “exacerbating their existing chronicity.” A limited number of overall COPD patients will maintain visitation schedules with their physicians.
A. The typical therapeutic regime for a COPD patient arriving at the hospital with an acute pulmonary infection is a tapering course of steroid therapy. The patient is also given a beta aerosol by power nebulization.
B. All too often, the patient has terminal bronchial airway narrowing caused by associated mucosal and submucosal edema which would require an alpha aerosol as a topical vasoconstrictor. Antibiotics may or may not be administered.
C. If the COPD patient is clinically desaturated by an acute pulmonary infection with an elevated PaCO2, a volume-pressure cycled (CMV) ventilator may be prescribed in an attempt to improve arterial saturation and blow off CO2.
D. The design application for volume-pressure cycled ventilators is in patient populations with essentially near normal lungs such as post-operative patients, thoracic injuries or patients requiring assistance or control to a depressed spontaneous respiration.
E. Barotraumatic consequences are elevated when pressure-volume cycled medical ventilators are used to mechanically ventilate patients with stiff inelastic lungs with variable diffuse endobronchial obstructions resulting in low gross pulmonary compliance.
F. Because alternative lung recruitment methods are not known or are not available to the prescribing clinician, more often than not, COPD patients with acute Bronchiolar airway restrictions and associated alveolar hyperinflation are ventilated (BY DEFAULT) with pressure-volume cycled ventilators with scheduled PEEP.
Volume-pressure cycled ventilators were designed to maintain pulmonary lung functions with very limited ability to recruit bronchial airways narrowed by retained endobronchial secretions with terminal mucosal and submucosal edema. When the functional limits and the potentials for barotrauma associated with volume-pressure cycled medical ventilators are carefully analyzed, their very limited lung protective strategies are exposed.
Certain recent medical literature infers that there is no alternative to the use of VOLUME-PRESSURE cycled medical ventilators with their accepted typical risk factors for treating acute COPD patients. This patient population can have major peripheral airway restrictions causing the narrowing of Bronchiolar airways by congestion caused by retained proximal endobronchial secretions as well as by terminal airway mucosal and sub mucosal edema.
The following documentation will reveal the limitations and risk factors associated with traditional VOLUME-PRESSURE cycled medical ventilators when they are used to ventilate low compliance obstructed pulmonary structures.
1. A volume-pressure cycled ventilator has limited primary options when ventilating a patient with low gross pulmonary compliance with peripheral airway obstruction and alveolar hyperinflation.
The primary volume-pressure ventilation programming options are:
2. A “volume cycled” ventilator is primarily scheduled to repetitively deliver a selected volume of a respiratory gas into the lungs under an arbitrary programmed peak positive pressure (PIP).
3. Essentially, this pressure is used to force the lungs to expand. If the selected pressure (PIP) is not sufficiently high to force the selected tidal volume into the lungs, thus failing to deliver the tidal volume selected, the ventilator becomes “pressure cycled.”
4. By scheduling a lengthened inspiratory inflation time, a breath hold at end inspiration (apneustic hold) can be programmed. Under apneustic hold programming, the ventilator is cycled on time under a selected peak inspiratory pressure limit (PIP).
Thus the lungs can be held inflated at pressures up to the selected peak delivery pressure (PIP) until mechanically time released.
The delivery of a programmed tidal volume under a selected pressure cycled schedule is only possible with a “cuffed” endotracheal tube. The cuffed endotracheal tube is designed to prevent ambient leaks in the ventilator inspiratory circuit and the conducting physiological airway. A non-leaking ventilator/ physiological airway interface must be maintained to allow accurate volume-pressure cycling.
5. The selection of a Positive End Expiratory Pressure (PEEP) serves to prevent the patient from exhaling (emptying) the lungs to the normal end inspiratory resulting position. The (PEEP) programming increases the Functional Residual Capacity (FRC) of the lungs (the amount of air left in the lungs by the next scheduled inspiratory phase).
6. When a positive end expiratory pressure (PEEP) is selected under a pre-selected tidal volume (with sufficient delivery pressure reserve), the selection of PEEP can cause an appropriate increase in the delivered tidal volume, which could lead to the hyper-expansion of certain lungs.
7. Generally, the greater the lung injury, the greater the mandated requirement for increased oxygen concentrations in the respiratory gases used to ventilate the patient (FIO2). The greater the clinical efficiency of the mechanical ventilator (all else being equal), the less the required FIO2 during the mechanical ventilation of the lung. It is well established that continuous inhaled oxygen concentrations over 40% become increasingly toxic with concentration (partial pressure) and increasing time.
In effect, by the selection of a moderate FIO2 for oxygen saturation and the maintenance of an effective intrapulmonary gas exchange to “wash out” carbon dioxide, a volume-pressure cycled (CMV) pulmonary ventilator, if properly programmed, can assist or control the pulmonary ventilation of a mammalian lung within limited compliance levels as well as non preferential airway obstruction.
A CMV pulmonary ventilator employing only an over pressure relief venting and alarming was not primarily designed with “lung protective strategies.”
As endobronchial obstructions associated with a decreasing gross pulmonary compliance increase, the greater the required tidal delivery pressures (PIP) required to deliver the selected tidal volume. The selection of a positive end expiratory pressure (PEEP) can further increase the potential for pulmonary hyperinflation.
The previous schematic demonstrates the causes of typical diffuse variable endobronchial airway resistances associated with acute and chronic pulmonary obstructional processes. This type of patho-physiology can occur as an acute episode triggered by induced intrapulmonary bacteriological or chemical agents as well as by COPD. Thus, the obstructive processes can be caused by cardiopulmonary disease as well as by induced airborne chemicals or biological agents.
Preferential pulmonary airways can lead to early alveolar air trapping and hyper-distension. Of considerable clinical importance is the recognition that the most patent airways serve the most dependent alveoli which, in turn, are at the highest risk of hyperinflation.
The volume-pressure cycled (CMV) ventilation of lungs with extensive forms of diffuse airway obstruction is almost certain to mandate preferential airway delivery leading to potential hyper-inflational barotrauma.
The introduction of Dr. Bird’s air-oxygen blender in 1963 allowed the precise Final Inspiratory Oxygen concentration (FIO2) selection during the mechanical ventilation of the lung. The Bird blender allowed the selection of either continuous therapeutic low free flows or high flows for positive pressure ventilation FIO2.
low free flows or high flows for positive pressure ventilation FIO2.
The above schematic demonstrates the physical principals involved when diffuse hyperinflational pressures attempt to equalize during a prolonged inflational interval causing barotraumatic consequences.
Barotraumatic time constants are dependent upon the gross pulmonary compliance and the existing type and degree of endobronchial airway obstruction. Pendeluft is a major cause of pulmonary barotrauma when volume-pressure cycling (CMV) ventilators are used to ventilate patients with acute intrapulmonary airway obstruction as well as advanced COPD patients with low gross pulmonary compliances.
By referencing the above schematic of a single alveolus inflated with increasing peak inspiratory pressures (PIP). As the cross section (diameter) of the alveoli increase, the alveolar wall thickness decreases to the final point of rupture. Secondary to mandated preferential airway, this is the route to mass hyper-inflationary barotrauma with a volume-pressure cycled ventilator. Thus the CMV volume-pressure cycled ventilator serves to accelerate flow through the preferential hyperinflationary pathway increasing potentials for lung injury.
OF IMPORTANT NOTATION: Under a 1976 510K grandfather-marketing clause, the volume-pressure CMV ventilators were released for public use by the US FDA Medical Device Act as being substantially the same as existing commercially available ventilators of that date. The FDA did allow the use of the later (beyond 1976) 510K substantiation “micro-processor state of the art” without required grandfather documentation.
The 510K marketing release for CMV ventilatory devices led to labeling changes. A classical example was the traditional “assistance to a spontaneous respiration” called “ASSISTED VENTILATION”.
This traditional labeling was changed to “SUPPORT VENTILATION” as a commercial means of insinuating a NEW FUNCTION being added to CMV ventilators. Existing volume-pressure cycled (CMV) ventilators, by US Federal Mandate, must comply with existing type devices commercially available on May 28, 1976.
At this writing, the sale of volume-pressure cycled ventilators is a multi-billiondollar industry. The same original FDA 510K marketing release has allowed the classical CMV volume-pressure cycled ventilators to advance from the displacement measured delivery of tidal volumes to the current Flow x Time = Tidal Volume programming.
With a general constant mechanical inspiratory flowrate during the inspiratory phase of available volume-pressure limited ventilators, as well as an associated low compliance breathing circuit, the induced inspiratory positive pressure rise is almost totally used to increase lung volumes. Thus, the gross pulmonary compliance (amount of give for the amount of push) will determine the required pressure rise to deliver the selected tidal volume or cycle on the selected peak delivery pressure (PIP).
When a mechanically generated intrapulmonary airway inflow meets physiological intrathoracic resistances, the constant inspiratory flowrate can be near instantaneously converted into an increase in the positive intrapulmonary delivery pressures. This intra-airway flow/pressure spike can create barotraumatic consequences within preferential (high compliance) Bronchiolar airways and the alveoli which they serve.
Hoop and circumferential stress describes how hyperinflation of the neonatal bronchial airways produces parallel airway tearing within the Bronchiolar wall and hyper-inflational barotrauma within the mature alveolar lung structures. Both of these barotraumatic events can be aggravated by elevated PIP selection or extended inflational time with certain volume-pressure cycled ventilator programming.
The MEAN INTRATHORACIC pressure during the mechanical ventilation of the lung plays a major role in the metabolic work done by the right ventricle of the heart. In chronic obstructive lung disease (COPD), the chronic resistance to blood being pumped by the right ventricle through the pulmonary capillaries to the left chambers of the heart serves to stress the right ventricle of the heart, ultimately leading to right heart failure called “Cor Pulmonale”.
All volume-pressure cycled ventilators with or without programmed positive end expiratory pressure (PEEP) programming serve to increase the MEAN INTRATHORACIC pressures, decreasing CARDIAC OUTPUT.
When the physiological Bronchiolar airways are hyperinflated by disease or mechanically by the use of an extended end positive pressure (PEEP), the intrathoracic pulmonary vessels including the pulmonary, Bronchiolar and lymph are stretched and narrowed. This reduction in vesicular caliber increases the resistance to flow within the vessels in proportion to the hyperextension of the elastomeric walls of the Bronchiolar Airways.
When chronic hyperinflation is created by obstructive pulmonary diseases such as an increasing bronchitis, the flow through the bronchial circulation serving to perfuse the peripheral lung structures is reduced, leading to a long-term progressive ischemia of the peripheral lung tissues creating the end stage lung disease called PULMONARY EMPHYSEMA.
Mechanical therapeutic control over pulmonary diseases causing hyperinflation must serve to break up the unrelenting hyperinflation of the Bronchiolar airways and the alveoli they serve. This must be done on a multiple daily basis, providing for both lung as well as circulatory recruitment. Without an adequate multi-daily Bronchiolar circulatory recruitment, the ischemic pulmonary disease process will cause an insidious necrotic end stage lung disease, called pulmonary emphysema.
The following circulatory drawing is designed to demonstrate the attachment of the pulmonary circulatory vessels to the pulmonary airways.
THE PRESENTATION OF THE PULMONARY CIRCULATION IS BY NETTER COURTESY OF CIBA® 1976
The preceding circulatory schematic serves to demonstrate venous (partially de-saturated) blood entering the pulmonary artery from the right ventricle of the heart. From the pulmonary artery, venous blood flows through the pulmonary capillaries adherent to the pulmonary alveoli.
As the venous blood traverses the pulmonary capillaries, oxygen molecules pass through the alveolar-capillary walls then through the blood plasma into the red blood cells. The re-oxygenated hemoglobin complex within the red blood cells transports the arterialized (re-oxygenated) pulmonary blood into the ventricle of the left heart to be pumped into the systemic (body) circulation for its role in metabolism.
Of major importance is the fact that when the bronchioles are narrowed (obstructed), peak inspiratory gases are trapped at end inspiration within the alveoli causing them to become hyperinflated (expanded).
As the alveoli become hyperinflated (expanded), the pulmonary capillaries firmly attached to the walls of the alveoli are stretched and narrowed, creating resistance to pulmonary blood flow from the right chambers of the heart through the lungs into the left chambers of the heart.
When a volume-pressure cycled ventilator increases the MEAN INTRATHORACIC PRESSURES, the resistance to blood flow from the right ventricle into the pulmonary artery is increased. This increases the work of the right heart, which can be already stressed or failing (Cor Pulmonale). Thus, the increase in MEAN INTRATHORACIC pressure created by the CMV ventilator programming creates a decrease in effective cardiac output.
All effective means of lung ventilation can reduce existing physiological cardiopulmonary dead space, which consists of:
1. In health, the cardiopulmonary functions maintain the constant regulated ventilation of the lungs by what is termed spontaneous breathing. VENTILATION.
2. Venous blood flows through the pulmonary capillaries where oxygen molecules diffuse across the alveolar/capillary blood gas interface to re-oxygenate the venous blood. DIFFUSION.
3. Blood flow through the pulmonary capillaries is provided by the automatic pumping action of the right ventricle of the heart which pumps the systemic venous blood it receives through the pulmonary capillaries. PERFUSION.
Any depressed component of the physiological dead space including Ventilation, Diffusion or Perfusion can cause CARDIOPULMONARY FAILURE. Existing volume-pressure cycled mechanical pulmonary ventilators (respirators) are primarily designed to mechanically manage ventilation. They can enhance oxygen diffusion across the blood/gas interface by increasing the oxygen content of the ventilator delivered respiratory gases (FIO2). By design programming mandate, CMV ventilators “increase the mean intrathoracic pressures”, thus potentially decreasing cardiac output.
While volume-pressure cycled ventilators (with all their available programming options) perform extremely well ventilating lungs with near normal compliance and limited airway obstruction, they were not primarily designed or modified to ventilate low compliance lungs with peripheral airway narrowing resultant from obstructive processes leading to alveolar hyperinflation.
Therefore, the potential for intrapulmonary barotrauma during volume-pressure cycled ventilation is accelerated in COPD patient populations or individuals experiencing an acute exposure to chemical or bacteriological agents. Either scenario will create an endobronchial-alveolar obstructive process causing major peripheral airway obstruction and associated alveolar hyperinflation with associated low pulmonary compliance.
Unfortunately, clinicians not familiar with optional forms of mechanical lung ventilation for high risk patient populations with obstructive pulmonary diseases or those who do not have these options available, accept the elevated mechanical ventilatory risk factors as current “state of the art”.
If you were among the some current 20,000,000 US citizens with COPD who may ultimately live or die based upon the clinical efficacy of the mechanical ventilator employed to keep you alive during the treatment of an acute pulmonary infection, would you not demand the current “state of the art” available in a Therapeutic Lung Recruitment (TLR™) ventilator?
Equally important, if you were to be among those who will be involved in a MASS CASUALTY (such as Asian avian influenza or induced chemical or biological agents which are described as having the potential to create major acute bronchial airway obstructions secondary to mucosal and sub mucosal Bronchiolar edema as well as retained proximal endobronchial airway secretions), would you demand an available therapeutic means of lung recruitment (TLR™) with a “lung protective strategy” in lieu of volume-pressure cycled ventilation “without a designed LUNG PROTECTIVE STRATEGY” as a defense against alveolar hyperinflational barotrauma?
HISTORY OF MEDICAL RESPIRATORS-
During the 1900’s there were three non-corporate individual biomedical researchers who were primary lifelong innovators in the concept and design of mechanical breathing devices.
1. Dr. Forreger was a primary innovator in the conception and development of anesthesia devices to support respiration in individuals under the influence of anesthetic agents and the manual ventilation of patients with depressed respiration.
2. Dr. Emerson made many conceptual and developmental innovations for the long-term ventilation of paralytic patients with depressed spontaneous respiration as well as in respiratory resuscitation devices and critical care ventilators.
3. Dr. Bird conceived and developed aeromedical pneumatic positive pressure breathing devices and anti g-suit regulators for airmen before he transitioned into the concepts and development of civil mechanical pneumatic cardiopulmonary breathing devices.
Now at 88 years of age, Dr. Bird continues to be conceptively active in 2009, devoting much of his time toward the teaching of pathophysiological concepts associated with obstructive lung diseases.
As early as 1943, Dr. Bird had, by conceptual design or circumstances, addressed several of the potential areas requiring “a lung protective strategy” in a mechanical respirator potentially designed for home care by patients with COPD.
Dr. Bird’s first manual Intermittent Positive Pressure Breathing device addressed the rate at which respiratory gases were delivered into the lungs to a peak pressure. The device had manually selectable “inspiratory- flowrates” controlled by the patient sensing how rapidly they expanded their lungs. This enhanced alveolar distribution of the delivered tidal exchange.
By means of a counter pressure caused by a physiological airway pressure rise against a diaphragm connected to the top manual inspiratory- flowrate knob, the patient was forced to taper the rate at which the lungs were terminally inflated. Thus the automatic counter pressure increased as the lung volume was manually increased, serving to progressively decrease the terminal inspiratory flowrate.
After seven prototype respirators and as many years of conceptual and developmental research, the universal neonatal through pediatrics to large adult Bird® Mark 7 Assistor Controller Respirator was placed into mass production. The Bird® Mark 7 respirator was designed from the most basic concepts to provide maximum clinical efficacies in the most challenging cardiopulmonary patient populations while providing for “lung protective strategies”.
The anesthesiologists with their hand powered anesthesia bag claimed they had an “educated hand.” While theoretically challenged in terminology, they could effectively manually ventilate congested lungs with very low gross pulmonary compliances without provoking pulmonary barotrauma. Dr. Bird’s design concept was to duplicate the ventilatory dexterity of the anesthesiolgist’s manual skills in an automatic pulmonary respirator.
Among the novel design principals employed to make the Bird Respirators more clinically effective while maintaining a continual “lung protective strategy” were:
1. A rotary airfoil called a venturi was designed to automatically vary the inspiratory flowrate by rapidly responding to physiological pressure changes retrograded from the lungs into the proximal venturi tube through the physiological endobronchial airways.
2. This logic served to prevent a rapid endobronchial airway pressure spike as physiological airway inflows which could cause a rapid potential dissecting intrapulmonary pressure rise were obstructed.
Dr. Bird’s concept for pneumatic venturi clutching continued to provide for major methods of maintaining a “Lung Protective Strategy” in four generations of Dr. Bird’s cardiopulmonary ventilatory devices.
While maintaining a projected “Lung Protective Strategy,”the selectable semiautomatic inspiratory FLOWRATE control conceived by Dr. Bird enabled the universal selection of the most clinically effective breathing pattern for neonates through pediatrics to large adults with lung injuries as well as for lungs with congestive airway obstructions.
The Bird respirators were designed to enter into an inspiratory phase if the patient did not take a spontaneous breath within a selected time. This provided for what is termed CONTROLLED RESPIRATION.
During controlled respiration, flow dampening was introduced to prevent an initial potential square wave endobronchial inflow which could impair alveolar distribution.
The amount of patient effort to trigger assistance to a spontaneous inspiratory breath was called RESPIRATOR SENSITIVITY. The amount of patient-created physiological inspiratory effort was selectable to decrease the work of breathing. Like controlled respiratory programming, the initial square wave potential was obtunded to maximize bilateral alveolar volume distribution.
DR. BIRD’S POST WW II AIRMAN’S ANTI-G SUIT REGULATOR
The magnetic clutches employed in Dr. Bird’s earlier airman’s anti g-suit regulator as well as the loading and dump valve switch logic were used to provide selectable sensitivity (synchronous lung ventilation) and peak pressure (PIP) limits on Dr. Bird’s designed pneumatic medical respirators. The concept of the pneumatic dump switch provided for a pneumatically servoed exhalation valve.
Dr. Bird designed an advanced nebulizer (Micronebulizer) based upon meteorological as well as physical principals and associated mathematics.
This concept improved site delivery of topical vasoconstrictor-bronchodilator aerosols within the peripheral Bronchiolar airways enhancing therapeutic lung recruitment in COPD patients.
Nebulizers conceived and designed by Dr. Bird were matched to the scheduled semiautomatic inspiratory flowrate of the respirator and the associated intrapulmonary volume delivery, maintaining a specific particulate spectrum within the operational pressure range and endobronchial airway patencies.
The termination of an inspiratory phase in a volume-pressure cycled respirator is dependent upon a non-leaking physical-physiological airway interface to allow the volume or cycling pressure to be reached. At times an ambient airway leak can occur in a volume-pressure cycled respirator’s breathing circuit preventing pressure rise cycling.
This limitation was addressed by Dr. Bird through a novel timed pneumatic flow accelerator. If the respirator’s pressure cycled inspiratory phase did not terminate at a scheduled variable inspiratory flowrate, a mechanical flow accelerator would gradually increase pulmonary airway inflow until it was sufficient to cover small to moderate ambient airway leaks, allowing the pressure cycling of the associated inspiratory tidal exchange.
Another important concept associated with terminal inspiratory flowrate acceleration was to initially (during a first stage inflation) gradually increase the internal diameter of the pulmonary airway cross section to prepare them for an increased inflow velocity, thus enhancing alveolar distribution while maintaining a limited “Lung Protective Strategy”.
The BabyBird® respirator conceived by Dr. Bird became available in 1969, creating a major decrease in neonatal respiratory deaths. In the years to follow Dr. Bird went on to conceive and develop a number of cardiopulmonary support devices.
In the early 1960’s, Dr. Bird became interested in the work Dr. Ralph Waters accomplished back in 1921 relating to his producing a pulsatile rise in systemic blood pressure by rapid cyclic lung inflation.
Dr. Waters essentially tightly wrapped the chest of a dead surgical table patient with bandages. He then ran a cut-down at the ankle level. With a competent airway intubation, Dr. Waters used the gas-flush on his anesthesia machine to rapidly inflate the lungs. During each inspiratory flush he noted a pronounced blood flow from the cut-down. Dr. Waters thereby substantiated the ability to create a controlled cyclic right to left vesicular peristalsis to blood flow within the pulmonary circulation. Additionally, the left ventricle was sufficiently compressed by lung inflation to produce arterial blood flow into the systemic circulation.
Note: Dr. Cournand et al., in the early 1950’s, described his Cournand #3 curve, which scheduled a positive I/E ratio with at least a 1.5 expiratory ratio during the mechanical ventilation of the lung. His rationale was that the left ventricular loading pressure was increased during the inspiratory phase by the positive intrathoracic pressure rise, at the expense of a decreased gross pulmonary blood volume. By increasing the expiratory time as opposed to the programmed inspiratory interval the right heart would have time to reload the pulmonary circuit, thus decreasing the potential for a chronic pulmonary hypovolemia.
The deleterious effects upon cardiac output associated with the mechanical ventilation of the lung is well known, at times proving to be the cause of death. This is currently accepted as “state of the art” by those who have created what they call “Evidence Based Medicine” as applied to volume-pressure cycled ventilator programming. This accepts the fact that in their “recognitions” rendered during the early years of the 2000’s, there were no alternatives.
In early 1978 Dr. Bird merged his wholly owned Bird Corporation into the 3M Company. He then entered into full time conceptual biomedical research at his existing Idaho Bird Space Technology Corporation facilities.
Dr. Bird et al. had created the Bird Respiratory Rehabilitation Center on the Palm Springs California Airport in the mid 1950’s. This was primarily a cardiopulmonary research center funded by public and private support. The goals of the facilities were to develop medical protocols that could maintain patients with left congestive heart failure and COPD in their homes, while ameliorating the symptoms of their diseases. This facility operated for over a quarter of a century treating as many as 200 patients daily with various pharmaceutical and mechanical protocols to ameliorate the symptoms of their various cardiopulmonary diseases. This produced a vast documentary learning curve relative to the evaluation and maintenance of the various forms of cardiopulmonary diseases.
By the mid 1960’s Dr. Bird’s wife Mary, who had long-term bronchitis, was becoming increasingly chronic with clinical revelations suggesting early pulmonary emphysema. This obviously served to cause Dr. Bird to become increasingly knowledgeable about the pathophysiology of chronic bronchitis leading to pulmonary emphysema and the potential clinical protocols directed toward the amelioration of the disease.
Dr. Bird well realized that all current therapeutic protocols were directed toward treating the effects of the obstructive pulmonary diseases and were not projected toward maintaining the diminishing bronchial blood supplies known to create a peripheral Bronchiolar/alveolar ischemia with progressive necrotic peripheral lung decimation (pulmonary emphysema).
In 1978, with his existing 1960’s academic references, Dr. Bird started an advanced research protocol directed toward controlling the effect of highly regulated intrathoracic positive pressures upon cardiac output.
Historically, Dr. Water’s pneumatic systole protocols had been refined by Dr. Bird and had been semi successfully applied during an earlier research study at the University of Pennsylvania.
When elastomeric fluid-containing physiological vessels with directional check valves are cyclically compressed by surrounding tissues, a forward fluidic pumping action is created. The process is technically referred to as “vesicular peristalsis.” This process is often referred to in the medical texts as a “venous pump”. The programmed compressional i/e (milli-second) ratios determine the effective re-loading time for maximum cyclic stroke volumes.
Within the thoracic cage (chest) there are three circulations with their vessels attached to the expandable (elastomeric) walls of the pulmonary airways.
These intrathoracic circulations include:
1. The BRONCHIAL circulation, which transports arterialized (oxygenated) blood from the left side of the heart down through the tracheobronchial airways to the peripheral lung structures which include the Bronchiolar airways and pulmonary alveoli. The arterialized bronchial blood circulation perfuses the capillaries of the bronchial circulation, with some 1 to 2% of the cardiac output.
2. The PULMONARY circulation transports venous blood from the pulmonary artery through the pulmonary capillaries for re-oxygenation and then to the left side of the heart to be pumped into the systemic circulation.
3. The LYMPH circulation transports all intrathoracic protein that is not recovered by the venules back into the systemic venous circulation. Thus the lymph circulation prevents pathologically retained interstitial protein from creating edema within and around the pulmonary structures.
The previous discussions of the three intrathoracic circulations serves to demonstrate the influence of phasic airway expansion and contraction upon circulatory flow restrictions. Note that when the pulmonary airways and alveoli expand, the attached vessels are stretched and narrowed creating resistance to flow within all three circulations.
When the intrathoracic lymph system is overwhelmed because of an incompetent physiological lymph pump (without compensation), retained interstitial protein can create interstitial (extra alveolar) edema.
Diffuse pulmonary airway obstruction can be a major component of gross pulmonary compliance. However, intrapulmonary interstitial edema can also become a major cause of a low pulmonary compliance.
For many years, Drs. Emerson, Bird and others had attempted to conceive a viable methodology to percuss the pulmonary structures from within to improve pulmonary airway secretion mobilization and clearance to the same (or beyond) levels achievable by chest physiology (chest clapping).
However, when rapid overlapping successive percussive bursts of sub tidal gas volumes were introduced endobronchially, they served to fire the intrapulmonary airway stretch receptors (Hering Breuer) into an immediate physiological expiratory effort. This response had long been called “bucking on the tube” by anesthesiologists and was associated with rapid sharp anesthesia bag compression in a lightly anesthetized patient.
Periodically over the many years, there has been a number of high frequency diffusive forms of lung ventilation introduced consisting of diaphragmatic vibrations, etc. These devices produced a repetitive high frequency diffusive shock wave into the patient’s proximal airway. The intrapulmonary oxygen diffusion was sufficiently active to cause an increase in therapeutic oxygen uptake as confirmed by PaO2 measurements. However, without a simultaneous convective intrapulmonary gas exchange to “wash out CO2,” an insidious increase in respiratory then PaCO2 saturations occurred.
Pure high frequency “intrapulmonary diffusion” (created by kinetic (vibratory) energy without displacement) is confirmed by the measurement (counting) of the instantaneous kinetic molecular movement in and out of a patient’s proximal airway, which must be exactly the same. The diffusion of oxygen molecules across the alveolar-capillary membranes into the hemoglobin complex is the primary method of intrapulmonary oxygenation.
In the 1970’s, Dr. Emerson introduced a high frequency gas injector in the form of a pulmonary ventilator, which was more capable than any other vibratory device previously developed. However, when an attempt to convert vibratory energy into the endobronchial injection of high frequency intrapulmonary “mini sub tidal volumes” was attempted, the Hering Breuer reflexes became active.
Dr. Bird initially directed his post 1978 conceptual research toward the development of a miniaturized respirator called a Phasitron® which was located at the proximal airway.
Additionally, a pneumatic flow/timing cartridge (ventilator) was required to phasically cause the respirator to inject sub tidal (small) volumes of a respiratory gas into the lungs with near instantaneous successive total valve opening to exhaust the injected sub tidal gas volumes to ambient from the unobstructed proximal airway.
Dr. Bird’s pneumatic Percussor respirator, called a Phasitron®, was capable of injecting clean repetitive subtidal volumes into the physiological pulmonary airways in under 3 milliseconds at injection rates of over 7,200 strokes per minute with clean 1:1 i/e ratios. These sub tidal intrapulmonary volumes were without inadvertent clinically detrimental positive end expiratory pressures.
The Phasitron® Respirator was cyclically servoed by a pneumatic remote time cycled ventilator cartridge capable of cycling at rates of over 7,200 cycles per minute.
Total valve opening and closing, with 1:1 i/e ratios, required under 6 milliseconds for each successive complete valve opening and closing.
THE PRECISE FLOW/TIMING LOGIC CELL FOR UNIVERSAL TIME CYCLED VENTILATION.
DR. BIRD’S UNIVERSAL MASS CASUALTY TXP™ RESPIRATOR
THE PHASITRON® AND LOGIC CELL WAVE FORMATS AVAILABLE IN A TIME CYCLED PERCUSSIONATOR (VENTILATOR) WITH AUTOMATIC POSITIVE i/e and I/E RATIOS.
The first modular pneumatic miniaturized device employing Dr. Bird’s novel fourth generation technology created a time cycled, FLOWRATE controlled ventilator (Percussionator®) which was designed for the routine ventilatory lung recruitment and maintenance of any size patient, anywhere, at any time. This became the Military Transporter™ Ventilator (TXP™). Characteristically, it would ventilate any patient capable of being mechanically ventilated equal to or better than any other existing pulmonary ventilator.
Over the years, the miniaturized universal TXP™ ventilator has proven to be a highly reliable miniaturized universal MASS CASUALTY transport as well as a routine ventilator for all patient populations.
It will function under water, after eight (8) g shock impactions, after major explosive aircraft cabin decompressions as well as under hypobaric conditions and/or in microgravity.
The TXP acute care module used in the Transporter™ Ventilator evolved into the universal pneumatic critical care Volumetric Diffusive Respiration (VDR®) concept. The VDR® Percussionator® (ventilator) became the integrated multi module matrix device during the FDA’s IDE-PMA studies. The VDR® employing the Intrapulmonary Percussive Ventilation (IPV®) concept has continued to effectively ventilate patients that have failed volume-pressure cycled critical care ventilators.
The VDR Percussionator design (with 34 pneumatic concomitant events) became the integrated VDR matrix device servoing the Phasitron Respirator (mechanical-physiological interface).
Thus a multi-modularized Percussive Percussionator (ventilator) has the scheduling capacities to effectively ventilate the smallest neonate through pediatrics to the largest adult capable of being mechanically ventilated while maintaining a LUNG PROTECTIVE STRATEGY.
The VDR® Percussionator® ventilator was placed into international clinical use in 1982. Since that time, the open VDR® programming options (with a Lung Protective Strategy) have allowed clinicians to successfully ventilate the most critical patients, from neonates through pediatrics to the largest adults, failing volume-pressure cycled CMV ventilatory programs.
The VDR-4® Percussionator® has proven to be the ventilator of choice in babies with severe cardiopulmonary compromises who are failing CMV and (push-pull) Oscillator ventilatory protocols. A classical use for the VDR® has been in the burn patient with associated inhalational injury.
ALLEGED EVIDENCED BASED RESPIRATORY CARE EXCLUSIONS
Pulmonary Patients who were excluded from the EVIDENCED BASED Mechanical Ventilation of the Lung:
1. They were younger than 18 years of age,
2. They were pregnant,
3. They had increased intracranial pressure,
4. Neuromuscular disease that could impair spontaneous breathing,
5. Sickle cell disease,
6. Severe chronic respiratory disease,
7. They weighed more than 1 kg per centimeter of height,
8. They had burns over more than 30 percent of their body-surface area,
9. They had other conditions with an estimated 6-month mortality rate of more than 50 percent,
10. They had undergone bone marrow or lung transplantation,
11. They had chronic liver disease (as defined by Child-Pugh class C).
SO HOW DO YOU CARE FOR THESE EXCLUDED CARDIOPULMONARY PATIENTS WHO COULD BE CRITICALLY INJURED BY AVAILABLE PRESSURE-VOLUME ORIENTED (CMV) VENTILATORS?
The answer is-
INTRAPULMONARY PERCUSSIVE VENTILATION (IPV®) and/or VOLUMETRIC DIFFUSIVE RESPIRATION (VDR®) WITH LUNG PROTECTIVE STRATEGIES.
NEONATAL BURN PATIENT ON A VDR PERCUSSIONATOR
HISTORICALLY, DR. BIRD’s INTRAPULMONARY PERCUSSIVE VENTILATION (IPVÒ) CONCEPT WAS NOT INITIALLY CLINICALLY INVESTIGATED IN FAVOR OF OTHER CLINICAL APPLICATIONS SUCH AS THE TXPÒ FOR ACUTE CARDIOPULMONARY STABILIZATION AND MAINTENANCE, OR VDRÒ FOR VOLUMETRIC DIFFUSIVE RESPIRATION FOR CRITICAL CARE VENTILATORY MANAGEMENT.
Both the TXPÒ and VDRÒ applications for Intrapulmonary Percussive Ventilation (IPVÒ) use obtunded (conservative) percussive flow/pressure endobronchial sub tidal injections for the recruitment of peripheral lung structures. The early TXPÒ and VDRÒ percussive lung inflation techniques did not employ the now current obtunded percussive amplitudes believed to be necessary for the rapid peripheral therapeutic lung recruitment of patients with acute and chronic peripheral lung diseases.
Unknowingly, this conservatism potentially exempted a major population of patients with acute and chronic forms of obstructive lung diseases from optimal resuscitative as well as daily peripheral lung recruitment. While Dr. Bird had spent many hours ventilating his own lungs with percussive amplitudes equal to what he believed would be required for optimal therapeutic lung recruitment, he remained reluctant to commence an early 1980’s on-patient study.
Dr. Bird’s wife Mary had been maintained on Intermittent Positive Pressure Breathing (IPPB) for what had transitioned from Bronchitis to chronic Bronchitis and then into pulmonary Emphysema with an Alpha 1 complication. At the point where Mary had entered into what was envisioned as an end stage acute pulmonary infection, Dr. Bird, without any other potential clinical resource, set Mary up for IPVÒ treatment with what he believed was a moderate percussive sub tidal delivery amplitude. Quite by accident (due to a pressure reduction regulator failure), Mary received what Dr. Bird considered at that time to be “a violent endobronchial percussion” with increased percussive delivery amplitudes he had only used previously on his own normal lungs.
The HARD percussion amplitude rapidly recruited Mary’s critically obstructive lungs. She continued multiple daily treatments (with HARD high impaction velocities), which enabled her to ameliorate her chronic lung disease to the point where she was again able to drive her car and perform many of her normal denied life style activities.
Following Mary’s clinical successes, Dr. Bird started five of his IPPB patients who were in what appeared to be advanced stages of COPD on a similar regimen. They all responded similarly to Mary’s remarkable experience with continuing improvement to the point where they were able to live near normal lives while remaining on the HARD amplitude settings on their home IPVÒ devices. They also did not display any outward signs indicative of any forms of pulmonary barotrauma.
While maintaining the same clinical protocols as her fellow COPD patients, Mary was insidiously becoming “activity limited.” She was emotionally distressed by seeing all five of her fellow COPD patients continuing to improve while she was deteriorating. The difference was that Mary had what was believed to be an Alpha 1 complication to her obstructive lung disease.
A classical oversimplified definition of Alpha-1 antitrypsin deficiency is that of a generic disorder characterized by the production of an abnormal protein. Low levels of the protein allow the destructive effects of “neutrophil elastace” to go unchecked, which results in damage to the delicate alveolar-capillary oxygen exchange tissues, thus interfering with the blood-gas oxygen exchange.
There is general agreement that the end stage lung disease Emphysema is caused by the destruction of the Bronchiolar circulation leading to an ischemic alveolar necrosis. Whether emphysema is caused by a progressive obstructive Bronchitis or accelerated by an Alpha-1 antitrypsin disorder or both remains to be further investigated.
What has been documented is that if a patient with a chronic bronchitis who is transitioning into early hyperinflational emphysema created by an associated bronchial circulation insufficiency (ischemia) with alveolar necrosis, continues with an optimal daily home IPVÒ therapeutic lung and circulatory recruitment, the insidious loss of Bronchiolar perfusion may be decreased of arrested.
It follows that if a patient with early Bronchitis follows a “daily prophylactic therapeutic protocol” directed toward peripheral airway recruitment and resolution of alveolar hyperinflation, the Bronchiolar circulation must maintain an enhanced perfussive function. This may explain why asthmatics, who experience acute (but not long term sustained) obstructive alveolar hyperinflation, do not become emphysemateous. Thus, an effective long-term therapeutic regime for patients with bronchitis may be directed toward routinely relieving the long-term Bronchiolar and Alveolar hyperinflation. Obviously, the earlier this therapeutic regime is instigated, the less the potential necrotic change secondary to unabating Bronchiolar-alveolar hyperinflation with the associated encroachment upon Bronchial blood flow.
Whether or not the associated Alpha-1 protein is the initiating rationale for bronchial blood flow impairment leading to pulmonary Emphysema, or whether it only accelerates the rate of a hyperinflational necrosis resulting in chronic bronchitis remains an unknown.
Lester Rumble, M.D. was an early patient with chronic Bronchitis transitioning into Emphysema secondary to repeated acute transient obstructive pulmonary infections.
Dr. Rumble and Dr. Bird’s wife Mary started IPVÒ therapy about the same time with what appeared to be the same extent of their COPD. Dr. Rumble continued to improve until reaching a point where he was able to resume a near normal level of activity.
Mary, while following the exact same therapeutic regime after her major improvement from an end stage pulmonary infection, continued to insidiously deteriorate. The only apparent difference between Dr. Rumble and Mary was that she had a suspected Alpha-1 handicap. However, Mary had been chronic long before Dr. Rumble became clinical. Thus Mary in all probability, had irreversibly lost a greater percent of her Bronchial circulation to hyperinflational ischemia.
Dr. Rumble oversimplified a rationalization (without any confirmation) that Mary’s continuing peripheral lung destruction was being caused by the peripheral lung deposition of the Alpha-1 protein from the bronchial and/or pulmonary circulations, which was challenged by a white cell (diapedesis action), which in turn could be a cause of an insidious Bronchiolar Alveolar necrosis. The alveolar protein deposition might be accelerated by restriAtive blood flow through either intra-thoracic circulation.
Dr. Rumble postulated that if Mary had been started on the clinically effective IPVÒ lung recruitment regime before her massive loss of Bronchiolar circulation had precipitated major Emphysemateous changes, her Alpha-1 complication might have been ameliorated, limited or arrested?
Early on, the most effective initial program for IPVÒ therapeutic lung recruitment was believed to be a period of percussive intrapulmonary mechanical mixing followed by an expiratory pause to an ambient baseline.
Later this was changed by spontaneously breathing through a continuous percussive wave format.
This intermittent percussion was followed by a continuous intrapulmonary percussion, with mobilization frequencies between 150 and 300 cycles per minute. Continuous percussion was then alternated with reduced secretion raising frequencies of 75 to 125 cycles per minute, with increased percussive amplitudes.
The apparent clinical efficacy of IPVÒ was attributed to the mobilization and airway clearance of retained endobronchial secretions while delivering a topical vasoconstrictor aerosol to reduce terminal brochiolar mucosal and sub mucosal edema, thus resolving Bronchiolar and alveolar hyperinflation.
Increasingly, IPVÒ programming has been directed toward further increasing Bronchiolar blood flow, hopefully reducing tendencies toward Bronchiolar-alveolar ischemia. This logic continued to be based upon Dr. Water’s initial 1921 work on “pneumatic systole”. During a lecture, Dr. Bird was asked how he was going to objectively prove the percussive sub tidal volume deliveries had “sufficient percussive amplitude” to increase the intrathoracic pressures to create a “venous type pumping action” within the intrathoracic circulations.
If this concept could be confirmed it would further explain the clinical efficacy directed toward the stabilization and apparent progressional arrest in many COPD patients who strictly followed the daily (home) use of IPVÒ for lung recruitment therapy.
Dr. Bird’s 1950’s circulatory schematic was advanced to examine the theoretical potentials for a possible effective intrathoracic Pneumatic Systole within the bronchial circulation (Intrathoracic Systemic Circulation). The percussive impaction pressure is well above the normal 15 to 35 mm Hg pressure drop between the arteriole and venule.
The check valves and or the higher arterial pressure could cause a peristaltic action within both the bronchial and the pulmonary circulations during a percussive intrathoracic sub tidal pressure rise.
The Phasitron® Respirator (located at the proximal airway) near instantaneoudly vents the proximal airways to ambient, creating a major distal to ambient flow gradient (with a near instantaneous pulmonary flow gradient reversal). Then, just before the partially obstructed peripheral bronchial-alveolar structures start to collapse, they are reinflated by the follow-on percussive endobronchial sub tidal delivery. This automatic i/e scheduling creates what may be called a “peripheral wedge pressure”. The scheduling produces a peristaltic change in pulmonary airway flow gradients in milliseconds as the sub tidal volumes are percussively injected, creating an expansion and contraction of the pulmonary airways resulting in an inverse peristaltic vesicular flow ehancement within their attached vessels.
A Pulmonary Catheter wedge and withdrawal serves to confirm the presence of a mechanical enhancement in the form of an “Intrathoracic Vesicular Persistalsis” to the physiological pulse wave during Intrapulmonary Percussive Ventilation (IPV®).
The rate at which the flow gradient reversal occurs enhances the “percussive shock waves preceding the delivery of an endobronchial sub tidal volume”. Thus the lung and circulatory recruitment of the intrathoracic pulmonary functions are influenced, by the rate of flow gradient reversal and the velocity (amplitude) of the Tidal Exchange. The near instantaneous proximal airway venting to ambient, enhances the elastomeric passive exhalation of the injected sub tidal volume. Thus it is the scheduled flow-pressure injection maintenance time that creates the percussive amplitude secondary to endobronchial resistances.
The above schematics serve to confirm logic that a 12 psi. obstructive PhasitronÒ jet pressure developed with a 40 PSIG selected operational pressure has a potential peak sub tidal delivery pressure as high as 150 cm H2O.
The clinical efficacy related to IPVÒ lung and circulatory recruitment (during the long term domiciliary management of COPD) may be capable of preventing an advancement of alveolar destruction secondary to Bronchiolar-alveolar hyperinflation and associated circulatory encroachments. “Intrathoracic vesicular peristalsis” may serve to further enhance blood flow through potentially restrictive vessels, reducing long-term ischemia and follow on bronchial-alveolar destruction (Pulmonary Emphysema).
Individuals, independently or under mass casualty conditions, exposed to an inhaled toxic chemical or biological agent, can develop a fatal acute peripheral airway obstruction.
The most immediately effective treatment for this type of lung injury is the recruitment of their obstructed lungs with Intrapulmonary Percussive Ventilation (IPVÒ). The home care ImpulsatorÒ can be powered by conventional house power. Backup power can be supplied by small 75 Watt AC generators or any source of a 50 psi 1.4 liter per minute flow of clean air.
THE HOME CARE SELF-CONTAINED HEAVY
IMPULSATOR® PERCUSSIONATOR®
Part # F00012-HT
IPV®-1C INSTITUTIONAL INTRAPULMONARY PERCUSSIONATOR®
Part # F00001-C
IPV® PERCUSSIONATORS® ARE POWERFUL HIGHER FREQUENCY LUNG RECRUITMENT VENTILATORS WITH AN INTEGRATED LUNG PROTECTIVE STRATEGY
Over the years ,the Hospital IPV®-1C and Home Care Impulsator® have continued to prove the clinical efficacy of Intrapulmonary Percussive Ventilation (IPV®) in terms of endobronchial secretion clearance and general ventilatory lung recruitment.
During home COPD therapeutic management, minor attention has been directed toward the potential role of “Intrathoracic Ventricular Peristalsis” during Intrapulmonary Percussive Ventilation (IPV®). As peripheral airway obstruction chronically advances in home care COPD patients, the secondary Bronchial circulation encroachment exacerbates (increases) the Bronchial-Alveolar ischemia, leading toward end stage lung disease (Pulmonary Emphysema).
The ability of IPV® to produce an augmentation to the physiological blood flow within the Intrathoracic Bronchial circulations with percussive IPV® programming continues to be academically confirmed. Dr. Bird has long suggested that the early (prophalactic) use of IPV® in the treatment of COPD could well reduce or limit chronic hyperinflational encroachments upon the Bronchial circulation.
Dr. Bird realized that the more rapid the Inspiratory-Expiratory endobronchial gradient transition, the greater the effective Intra-thoracic Vesicular Peristalsis. However, he was limited by the millisecond management of the percussive regulated operational air pressures. In other words, the limitation was the rate at which expiratory sub tidal outflow pressure at the proximal airway could be reduced to ambient.
The current home care IPV® logic (while highly clinically effective) requires an excess flow pressure gradient pressure maintenance to deliver a scheduled sub tidal volume. Thus, upon inspiratory-expiratory flow gradient reversal, a slight inertial delay is mechanically mandated before the proximal airway flow/pressure can be near instantly decreased to ambient.
Therefore, the effective circulatory pulse wave is more related to the millisecond rate of flow gradient reversal than the pressure differential. While this knowledge was known to Dr. Bird for many years, he had not conceived a method of managing inertial resistances during cyclic pressure gradient reversal in the self contained home care IPV® Percussionator .
Over time, Dr. Bird had conceived a pneumatic flow/pressure resistance system, to reduce the post sub tidal millisecond initial pressure drop delay to Ambient. However, a means for a flow/pressure balance, controlled by the rate of compressed air generation and utilization was not technologically available.
Finally, early in 2007, Dr. Bird had conceived the logic and developed a working prototype of a light-weight version of the existing Impulsator home care Percussionator. Thus the Home CARE HT™ Impulsator® with an advanced means of creating a more effective Intrathoracic Vesicular Peristalsis was created.
By early in 2009 over two years of on patient studies have confirmed therapeutic efficacies in terms of Bronchiolar and Alveolar Lung recruitment equal to or better than the existing heavy IPV® Impulsator. Mass production of the light-weight HT™ Impulsator® and distribution will be scheduled for later in 2009.
The general presentation of the HT™ IMPULSATOR® is as follows:
THE PERCUSSIONAIRE® Home Therapy (HT™)
Universal Bi-phasic IMPULSATOR®
Universal Bi-phasic (HT™) IMPULSATORÒ F00012-HT
Self Contained Home or Hospital Travel pack for Bi-phasic IPVÒ
Travel the world with the IPVÒ HTÔ IMPULSATORÒ Respirator discreetly contained in a protective camera-type travel case and weighing less than 15 pounds (7.5 kg).
This unit is available in special engineered compressor models powered by 110 volt 60 cycle or 220 volt 50/60 cycle AC or by emergency 12 volt converters or small emergency power plants.
EQUALLY IMPORTANT- the (home or travel) HTÔ IMPULSATORÒ provides the same IPVÒ lung recruitment therapy (any where, any time) you could receive in any major hospital if you were admitted with an acute cardiorespiratory infection, further increasing your clinical independence.
Additionally, the HTÔ IMPULSATORÒ
is the only transportable cardiopulmonary VENTILATOR designed for Bronchiolar and Alveolar lung recruitment as well as for potentially providing
MASS CASUALTY “LIFE SUPPORT”
WAVE FORMAT REVEALING PATIENT CONTROLLED Bi-phasic™ CHANGES
IN PERCUSSIVE AMPLITUDE DURING THERAPEUTIC
INTRAPULMONARY PERCUSSIVE VENTILATION (IPV®).
© Bird Institute of Biomedical Technology 2009
This educational documentary history was prepared by the BIRD INSTITUTE OF BIOMEDICAL TECHNOLOGY using data from standard textbooks and researching documents prepared over the many years by Forrest M. Bird, M.D., PhD., ScD. as well as his pathophysiological textbook resources.
Document ID: F-061309 FMB
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