Deane Hillsman, M.D.
University of California at Davis, Pulmonary Department, Sacramento, California, USA

The Rescue Breathing Pattern (RBP) is a universal cognitive response to dyspnea distress. Simply stated, the RBP is to "pump air in and out of the lungs as fast as you can."

For patients with Restrictive Lung Disease the RBP is a proper physiologic response, and the breathing pattern is dictated by a reduced and inelastic pulmonary reservoir.

In Obstructive Lung Disease, and particularly with Emphysema and loss of lung elastic recoil, the RBP is an improper response as it will lead to Air Trapping and Dynamic Hyperinflation. Overinflation places the chest bellows mechanism in a position of mechanical disadvantage and will independently exacerbate the dyspnea sensation. These physiologic principals may be understood by a consideration of the Flow-Volume Loop and in particular the static Pressure-Volume Curve.

To prevent and correct overinflation the COPD patient must breathe slowly, with a larger Tidal Volume, a prolonged expiratory phase, and breathe gently. This corrective breathing pattern is 180 degrees out of phase with the RBP. The RBP is therefore a corrupting reflex in COPD.

The commonest complaint in COPD is dyspnea, usually after an event of exertion or uncontrolled coughing. Frightened patients commonly activate the RBP which will in turn further exacerbate their dyspnea. This leads to a feeling of loss of control, and will compound their psychologic problems. When COPD patients learn to control the RBP they usually regain a significant measure of psychologic control.

Conclusion: The RBP is a universal response to dyspnea, and in COPD is a corrupt response leading to further dyspnea and a sense of psychologic loss of control. Control of the RBP in COPD will improve dyspnea and help to restore confidence and loss of control.

The Rescue Breathing Pattern ("RBP") is a cognitive universal response to acute dyspnea, or a dyspnea exacerbation of chronic dyspnea. It is a modulator of the usual regulatory feedback mechanisms of breathing control.

Simply stated, the RBP is to "...pump air in and out of the lungs as hard and as fast as possible..." in an attempt to relieve dyspnea distress.

The response is easily observed in normal subjects, both deconditioned and well conditioned athletes. It may also be seen in diseased patients, though the signs may be more subtle. It is seen in all varieties of lung disease, both airway obstructive and pulmonary restrictive diseases. It is also seen in all types of cardiac diseases, or any other miscellaneous conditions that produces dyspnea.

The only partial exception to this RBP rule is the general class of Anxiety Psuedodyspnea and/or Hyperventilation Syndrome. Note that these conditions are also cognitively driven, and frequently productive of erratic or bizarre breathing patterns. However, I submit that even the most anxious Hyperventilation Syndrome patient, if obliged to run 500 meters as fast as possible, or if submerged in their swimming pool for two minutes and coming up for their first breath of air, will exhibit the RBP at least initially.

The RBP is therefore a cognitive modulator response that is superimposed on the many reflex feedback breathing control mechanisms, such as the oxygen and CO2 sensors, chest wall and lung pressure and proprioceptive receptors, and many other receptors and their feedback mechanisms. Without question, these numerous feedback mechanisms are dominant and controlling in the regulation of breathing. The Rescue Breathing Pattern is not a competing theory of breathing control, but rather an adjunct modulator response to basic controlling mechanisms.

The Rescue Breathing Pattern is characterized by:

• Increased Respiratory Rate
• Increased Tidal Volume (Note: This is Rate limited)
• Forced Breathing ((Both inspiration and expiration)
• Increased air flow
• A focus on inspiration
• Shortened expiration time

I submit that almost everyone is subconsciously aware of the RBP. This can be demonstrated by asking yourself, or most medically untrained people selected randomly, the following questions regarding the RBP:
"What do you do if you are short of breath?" followed by:
"And what else do you do?" (In order not to provide inappropriately leading questions).

Almost everybody will easily reply to these questions that they breathe faster, with larger breaths, and attempt to breathe forcefully. Only a few will recognize increased air flow (though this is inherent in the reflex). Many will recognize their efforts are mainly directed to breathing in, though this may require some prompting such as "Do you find that you are working harder to breathe in or out." Only a relative few subjects will recognize a shortened expiratory phase, unless given quite leading prompting.

The author finds it very curious that this easily observable Rescue Breathing Pattern appears to be unrecognized in the pulmonary and psychophysiology literature.

Note the Rescue Breathing Pattern when contrasted to the mechanical breathing requirements of patients with COPD, Emphysema, and moderately severe/severe Asthma:

NORMAL (Rescue Breathing Pattern)	REQUIREMENTS for COPD / Emphysema / severe Asthma
Rapid Rate	Slow Rate
Large Tidal Volume (Rate limited)	Large Tidal Volume (Not Rate limited)
Forced Breathing	Gentle Breathing (N.B. Expiration)
Increased Air Flow	Decreased Air Flow
Focus on Inspiration	Focus on Expiration
Short Expiratory Time	Long Expiratory Time

Note that the RBP is essentially 180 degrees out of phase with the physiologic needs of the patient with COPD and severe Asthma, and particularly so in patients with Emphysema.
The Rescue Breathing Pattern is therefore a corrupt reflex in these COPD patients.

It is important to note however, the RBP is a physiologically appropriate response for patients with Restrictive Lung Disease.

Restrictive disease by definition is one that has limited the lung volume. The classic example is Pulmonary Fibrosis, and probably the most common example is cardiac disease with congestive heart failure. Here the limited pulmonary volume is being used to near capacity, i.e. working at the limit of the available elastic reservoir. This is why these patients typically have a rapid and shallow breathing pattern with a short expiratory phase, because this is the most mechanically efficient way to breathe under these constraints. Stretching this limited elastic reservoir further with large breaths will cause the Work of Breathing to increase markedly, and therefore cause further respiratory distress.

The RBP is in synchrony with the mechanical needs of these patients, and therefore is appropriate and should not be altered by breathing re-training.

In treating patients with Restrictive Disease do not attempt to alter the native rapid and shallow breathing pattern. The slow and deep breathing patterns taught by many breathing advocates are contrary to physiologic requirements. Calming and relaxation techniques, and coping strategies are appropriate, but altering native breathing patterns is detrimental to these particular patients.

It is instructive to read the definition of "GASP," as in "Gasping for breath" in non-medical dictionaries. Most definitions of gasp are related to theatrical descriptions, as in "...she gasped when she saw her husband in the arms of another woman..." and so on. However, there are a number of more physiological descriptions of interest.

The Random House Dictionary describes:

• "To struggle for breath with mouth open."
• "The long-distance runner gasped for air: struggle with open mouth (for breath), inhale frantically, labor for breath; suck in (air), breathe convulsively; have trouble breathing, respire laboriously; gulp, pant, wheeze, puff, catch the breath."

Webster's Dictionary describes:

• "To open the mouth wide in catching the breath; or in laborious respiration; to labor for breath; to respire convulsively; to pant violently."

It seems clear from these various descriptors that the lay public has considerable insight into, and recognition of, the Rescue Breathing Pattern.

Stedman's Medical Dictionary does not define the word "gasp," which appears to be a curious omission. Could this perhaps reflect that patients have been smarter than their physicians in recognizing the Rescue Breathing Pattern?

It is now necessary to consider some basic pulmonary physiology and mechanics of breathing, related to the conditions of "air trapping" and functional lung "overinflation," and this in turn related to the question of so-called "breathing exercises."

The 1955 seminal and classic textbook of pulmonary physiology THE LUNG by Dr. Julius Comroe (THE LUNG: Clinical Physiology as Pulmonary Function Tests - Julius H. Comroe et al, 1st. Edition, 1955) makes reference on page 127 in the section on Mechanics of Breathing to the phenomenon of "air trapping" and "...overdistention of the lung..." which "...may be noted to an even greater degree in emphysema..." The authors then went on to state "...If patients with air trapping are taught to breath out slowly, then can often breathe out more completely. This is one of the rational objectives of breathing exercises..."

It seems clear that the concept of air trapping and its detrimental consequences, and particularly so in Emphysema, has been well established for a long time.

However, the subject of "Breathing Exercises" has been a controversial one, as articulated by the 1992 statement from the European Respiratory Society:
"...until more definitive evidence is available, breathing training cannot be recommended in COPD..."
(Pulmonary Rehabilitation in Chronic Obstructive Pulmonary Disease (COPD) with Recommendations for its use - Donner, CF, Howard, P; European Respiratory Journal, 5, 266-275, 1992)

This author would like to point out that there are many types of Breathing Exercises, as seen for example with:

• Chest mobilization techniques (several varieties).
• Respiratory muscle strengthening exercises A.) Strength training B.) Endurance training (several varieties of each).
• Diaphragm awareness and use (several varieties).
• Thoracic - Diaphragm coordination (several varieties).
• Hyperventilation Syndrome (several varieties).
• Cervical fracture - chest paralysis (several varieties).
• Yoga / Meditation / numerous non-medical techniques.

It seems clear that the term "Breathing Exercises" means many things to many people, and as generally used is an almost meaningless term. As such it is not surprising there is controversy surrounding this subject. Any rational discussion of Breathing Exercises requires a precise definition of what one means by Breathing Exercises, and precisely what one is doing in that domain of interest.

The authors definition of "Breathing Exercises" relates to the therapeutic Breathing Pattern associated with COPD / Emphysema / severe Asthma which is, breathing pattern training (in conjunction with chest physical therapy techniques) that promotes the minimal necessary level of Alveolar Ventilation in conjunction with minimal Work of Breathing.

While empirical knowledge strongly suggests this pattern is one of a slower respiratory Rate, a larger Tidal Volume, a prolonged expiratory phase, and non-forced respiratory effort, the precise definition of the optimal Breathing Pattern / Breathing Exercise has yet to be defined by advanced pulmonary mechanics studies. Indeed, the precise ventilatory pattern may be found to be somewhat variable between different patients (See: Hillsman 1995 ISARP presentation).

Undisputed is the need to prevent and/or correct Air Trapping and Functional Overinflation.

The optimal Breathing Pattern must be achieved within the constraints of appropriate Chest Physical Therapy techniques, a discussion of which is beyond this presentation. These Physical Therapy questions in turn relate to frequently distorted chest wall configurations and associated respiratory muscular dynamics, an emerging area of research. In addition, the author intuitively believes the prolonged expiratory phase is associated with critically important respiratory muscle rest, which remains an unanswered question dependant on yet to be developed methodology to measure respiratory muscular "rest."

The normal bronchus is surrounded by and attached to a dense mesh of alveolar structures, which have elastic properties, largely due to embedded elastic fibers. These elastic structures constantly pull in all directions on the small airways, therefore helping to maintain open airways.

On expiration, with the chest decreasing in volume, all structures in the chest decrease in size. Alveolar volume decreases and air is normally evacuated, but simultaneously the airways also decrease in size. However, because of the normal elastic recoil properties of the surrounding lung, the relative degree of bronchial collapse is minimized.

In contrast the Emphysema patient has lost alveolar structure and elastic recoil properties. On inspiration there may be difficulties due to irregularities and distortion within the small airways, but the major problem is on expiration. Here the lack of elastic recoil results in excessive collapse of the smaller airways. Therefore the Time Constant for alveolar emptying must be prolonged.






The result is a basic need for a prolonged expiratory phase in COPD, and particularly so with Emphysema. Failure to achieve a longer Time Constant will result in Air Trapping and Pulmonary Overinflation.

This diagram is a simplistic reduction of the lung to one alveolus and its smaller airways within the surrounding chest wall.

On expiration the chest wall volume decreases, therefore applying relative pressure on the Alveolus, and thus promoting air flow through the airways.

However, at the same time pressure is also being applied to the smaller airways, and at some time a Critical Closing Pressure will be achieved, and at some point in the system the smaller airways will collapse and expiratory air flow will be further impaired.

Forced expiratory efforts will exaggerate the problem of Dynamic Bronchial Compression and further impair expiration. The result is a basic need for non-forced, gentle expiratory efforts.

The mechanical consequences may be appreciated by examining the familiar Flow Volume Loop.

Here a normal resting ventilation pattern is superimposed on the forced expiratory Flow-Volume Loop.

Note the normal subject has a relatively low FRC and therefore the ability to take in a much larger breath. Also note the normal subject has a much larger reserve of forced expiration as there is no airway obstruction.

In contrast, the severe Emphysema patient has a diminished capability to take a deep breath as the FRC is elevated, and likewise a much diminished capability of forced breathing due to airway obstructive disease. Therefore, the breathing reserve of the Emphysema patient is much diminished, and even with resting breathing these patients may be working near their available maximum reserve capabilities.

The mechanical consequences may be better appreciated by examining the Static Pressure-Volume Curve.

This curve is obtained by placing an esophageal balloon to measure the pleural pressure, and then having the subject inhale and exhale to several different lung volumes, with the glottis held open in a relaxed position. This measures the Transpulmonary Pressure, and is a reflection of the elastic recoil within the lung at different volumes.

Note in the normal subject because of the low FRC there is a large volume reserve to Total Lung Capacity. Resting breathing is accomplished with only a slight degree of effort, i.e. with only s slight degree of inspiratory pressure needed, and even a moderately large breath is achieved with only slight increased effort.

In contrast the Emphysema patient (for convenience shown on the same P-V Curve; the actual Emphysema P-V Curve is up and to the left and therefore with even more mechanical constraints) is working under great mechanical disadvantage. Even with resting breathing these patients are near their available Total Lung Capacity, and particularly if they are at or near the curvilinear position of the P-V Curve all breathing must require a much larger degree of effort.

This is because the chest wall and the respiratory muscles are in positions of mechanical disadvantage and operating inefficiently. Any attempt to take a deeper breath can only be as a result of excessive mechanical effort.

Note that with Functional Overinflation the patient will shift up the Pressure-Volume Curve and their mechanical breathing problems will therefore be greatly compounded.

The clinical problems of overinflation have been known for a long time, as elegantly shown with simple methodology in a 1958 paper by Dr. William Miller.

Air Trapping and Functional Overinflation is shown with exercise, and prevented by appropriate "Diaphragmatic Breathing" techniques.

Note particularly in the example of voluntary hyperventilation within only seven breaths a patient Air Trapping 1230 cc of air. Indeed, a striking example of how quickly significant overinflation, and therefore rapid decompensation, can develop.

Also shown is an example of Air Trapping with uncontrolled coughing, a very common problem causing respiratory distress in COPD.

More recent sophisticated studies by Michael Belman and colleagues (Inhaled Bronchodilators Reduce Dynamic Hyperinflation during Exercise in Patients with Chronic Obstructive Pulmonary Disease - Belman MJ, Botnick WC, Shin JW; American Journal of Respiratory and Critical Care Medicine 1996;153:967-75) as well as Denis O'Donnell and colleagues (Breathlessness during acute bronchoconstriction in asthma - Lougheed MD, Lam M, Webb KA, O'Donnell DE; American Review of Respiratory Diseases 1993; 148: 1452-1459 and Exertional breathlessness in patients with chronic airflow limitation - O'Donnell DE, Webb KA; American Review of Respiratory Diseases 1993 148:1351-1357) have given insight into the critical importance of dynamic Functional Overinflation in COPD / Emphysema / Asthma.

There can be no reasonable dispute as to the importance of Air Trapping and dynamic Functional Overinflation in the production of dyspnea in COPD / Emphysema / Asthma.

CHRONIC DYSPNEA

It is well established that chronic dyspnea may produce anxiety, depression, and a number of stress related psychological problems.

ACUTE DYSPNEA

Recurring acute dyspnea attacks are painful experiences, and it is understandable that patients frequently live in fear of these attacks. Fear of dyspnea attacks, and of the unknown, leads to a Loss of Control. The loss of control involves loss of the means to control the attack itself. Perhaps even more profound is the loss of control of "self," and the very basic qualities of what comprises the human experience.

The ability to control acute dyspnea attacks restores patient confidence over the most distressing component of the COPD disease process, which in turn can restore the loss of control of "self." Restoring "self" can have a profoundly positive effect on the patient's general outlook and well being.

A visual biofeedback training system was presented at the ISARP meeting in Toronto in 1995 and therefore this will not be elaborated on at this presentation (See: Hillsman 1995 ISARP).

Briefly, by menu selection an infinite variety of inspiration and expiration breathing patterns may be displayed on a computer CRT. A cursor blinks along the programmed line, and the patient attempts to match their real time performance with the programmed line. Performance deficiencies, such as the slow inspiration rate shown in the diagram, are immediately apparent and the patient is therefore given a visual biofeedback signal to correct their training performance.

A version of the program done in the LabVIEW environment is available at http://www.sierrabiotech.com

It is emphasized that while the analog displays may appear simple, the information content of visual analogs is high. This display method is a paradigm shift in respiratory diagnostic and therapeutic technology, in that the clinician can literally watch the patient breathe.

One significant point about the visual training system realized since the 1995 ISARP presentation deserves particular mention, and that is the importance of the AUTOSCALING display.

Note in the diagram the three displays are identical, due to autoscaling, but in fact while the breathing patterns are identical, they represent three very different breathing performances varying from 100 to 3000 cc Tidal Volume and 25 to 6 breaths per minute respiratory Rate.

In order to perform correctly, the autoscaling display forces the patient to focus on internal sensing of the biofeedback experience.

It is theorized this is why the autoscaled display appears to be a particularly effective respiratory biofeedback training tool.

It is speculated that autoscaling displays may be useful in other modalities of biofeedback training, such as Hyperventilation Syndrome.

The diagram is an actual patient record from the original visual biofeedback device in an individual with COPD.

On the top screen the patient display is blanked, to record the native breathing pattern in a standard manner (Tidal Volume 1000 cc, Rate 10 bpm).Note the patient Tidal Volume of about 500 cc, and a long expiratory phase, but despite this expiration does not return to the FRC baseline. This is Air Trapping, and in this example about 250 cc.

The lower screen is a prompted display. This is the patient's first training session, eight minutes later. Note the patient breathing pattern almost perfectly matches the desired program, with only a slight delay in starting inspiration. Annotations are made e.g. "You can breathe deeply" (the patient now achieving a Tidal Volume of 1150 cc) and "You can get the breath out" (the patient now exhaling down to resting FRC). Note the home instructions to the patient.

Patients are given a copy of their breathing record, and instructed to practice breathing twice daily, and for no more than five minutes (to avoid fatigue and boredom). They were told to sit in a comfortable chair, relax, and to concentrate on their breathing program and to "Put the picture in your mind." Depending on the situation various Physical Therapy techniques may be employed. Note carefully, this breathing pattern training will prevent Air Trapping. The usual patient demonstrates substantial retention of the breathing pattern prescription within two to three months. Note this training method is an example of Positive Reinforcement Biofeedback (i.e. the subject feels better with the biofeedback experience, and therefore the biofeedback is reinforced) which is inherently a more powerful biofeedback technique.

Typically a new patient is seen about three times in the first three months during regular office follow-up, with training sessions lasting about 10 to 12 minutes. While the learning rate is perhaps slower than other methods, the burden of training is almost entirely on the patient. As such, this method is exceptionally cost effective.

ISARP literature has posed the following research priority questions regarding Breathing Patterns:

1.) Can Breathing Patterns be learned?
The answer is YES, at least in an elderly COPD population, and with the anticipation that a younger Hyperventilation Syndrome population would also be trainable. Furthermore, it is surprisingly easy to teach the elderly new Breathing Patterns.

2.) Can Breathing Patterns be retained?
The answer is YES, at least in an elderly COPD population, but with retention lost to a variable degree over time. Generally two or three re-training sessions a year restores the learned pattern, though the occasional patient will retain their learned patterns for a year or more. Furthermore, spouses often report that after approximately three or four months the patient appears to be breathing in the learned manner while sleeping. If this observation is confirmed by sophisticated sleep studies it would strongly suggest that indeed learned Breathing Patterns are being retained. And this would also suggest that perhaps learned Breathing Patterns may be chronically and subconsciously influencing the general regulatory control mechanisms of breathing.

3.) Can Breathing Patterns be used clinically, outside the laboratory?
The answer is YES, at least in an elderly COPD population. The present proof of this is the time honored "clinical trial" or "therapeutic trial" as indeed the learned breathing patterns and techniques directed specifically at preventing and/or correcting pulmonary Air Trapping and Overinflation are clinical trials, and patients report success. Sophisticated ambulatory monitoring studies to confirm these patient reports would be highly desirable.

CONCLUSION: The Rescue Breathing Pattern is a common and important factor, and a corrupting cognitive response in COPD / Emphysema / and severe Asthma which produces exaggerated acute dyspnea events.

Dyspnea exacerbations are the commonest patient complaint in symptomatic COPD. The resultant adverse physiologic consequences of Air Trapping and Functional Overinflation may be prevented and corrected by appropriate Breathing Pattern training methods.

A system to train patients in appropriate Breathing Patterns to prevent and correct Functional Overinflation has been developed.