This document discusses dysfunctional breathing and its effects on physiology and psychology. It covers topics such as: - Dysfunctional breathing behaviors can compromise respiration, physiology, and psychology through learned habits. - Conditions like behavioral hypocapnia (low carbon dioxide levels from overbreathing) and hypercapnia (high carbon dioxide levels) can impact pH regulation and health. - The balance of carbon dioxide, regulated by breathing, and bicarbonate, regulated by the kidneys, work together to maintain the proper acid-base balance in the body as described by the Henderson-Hasselbalch equation.

1. Educational Capnography
DYSFUNCTIONAL BREATHING
Effects of Compromised Respiration
on Physiology and Psychology
Peter M. Litchfield, Ph.D.
Graduate School of Breathing Sciences
Tel: 307.633.9800 Cell: 505.670.2874
www.breathingsciences.bp.edu
pl@breathingsciences.bp.edu
Copyrighted 2012-2013

2. MISSION
Applied Breathing Sciences
Our mission is to help people
improve health and performance
through the application
of behavioral learning principles
to breathing physiology.
2

3. PROBLEM
Self-defeating learned breathing behaviors compromise
physiology, psychology, health, and performance.
Learned dysfunctional breathing has a major impact
on multiple physiological systems, resulting in
symptoms and deficits, usually attributed to other causes,
by clients and their health practitioners, rather than to learned
behaviors and responses that may account for them.
3

4. OBJECTIVE
Applied Breathing Sciences
Clients learn new breathing habits,
and related behaviors, that are consistent
with healthy physiology and psychology.
4

5. SOLUTION
Applied Breathing Sciences
Practitioners offer client-centered learning solutions,
based on the principles of:
● behavioral counseling
● behavioral analysis
● behavior modification
● cognitive learning
● awareness training
● applied psychophysiology
● phenomenological exploration (consciousness)
5

6. RELEVANCE
Breathing Learning Services
Dr. Robert Fried comments as follows:
“There are varying reports of its *dysfunctional breathing+ frequency in the population
at large, ranging between 10 percent and 25 percent. It has been estimated to account
for roughly 60 percent of emergency ambulance calls in major US city hospitals.”
(Fried, Robert Breathe Well, Be Well. 1999, p 45)
“Fewer than 1 in 100 of my clients show normal PCO2. It has long been known that it is
rare among persons with seizure disorders, heart disease, asthma, anxiety, stress, panic
disorder with or without agoraphobia, other phobias, hyperthyroidism, migraine,
chronic inflammatory joint disease with chronic pain, and so on, NOT to hyperventilate.
We’re probably looking at half the U.S. population.”
(The Psychology and Physiology of Breathing. 1993, pp. 43-44.)
6

7. RESPIRATION AND BREATHING
are not the same thing.
Respiratory physiology is reflexive.
Respiration involves the breathing mechanics of gas exchange (external respiration), the
biochemistry of gas distribution to and from tissues (internal respiration), and the
utilization of oxygen by the mitochondria of cells (cellular respiration).
Breathing physiology is behavioral.
Breathing is mechanical; otherwise known as external respiration. It is about moving air
in and out of the lungs. It is a behavior, however, that serves multiple objectives, such as
moving air to create speech. Breathing behaviors that serve these other objectives should
operate in concert with its primary objective, respiration.
Breathing, as a behavior, is subject to the same principles of learning as any other
behavior, including the role of motivation, emotion, attention, perception, and memory.
Failure to make this distinction between respiration and breathing has led to
fundamental misunderstandings that have prevented the practical union
of respiratory and behavioral sciences.
7

8. BREATHING OBJECTIVES
Breathing as a set of behaviors serves physiological, psychological, and social
needs and motivations. Here is a list of some of them:
● Delivery and utilization of oxygen (respiration)
● pH regulation, electrolyte balance
● Vascular regulation, e.g., cerebral and coronary
● Buffering metabolic acids, e.g., lactic acid
● Non respiratory lung functions (filtering and metabolic functions)
● Muscle regulation, e.g., triggering and dysponesis
● Defensive posturing, e.g., coping with stress and anxiety
● Speech and singing
● Psychological state changes (dissociation), disconnecting
● Emotional and mood control
● Secondary gain (benefits from symptoms)
● Sense of control, security, confidence
● Access to other responses, e.g., relaxation
● Meditation, consciousness shifts
● Yoga, consciousness shifts
8

9. BREATHING BEHAVIORS
Breathing behaviors are considered dysfunctional based on their relationship with other
behaviors and how together they impact physiological and psychology.
Here are examples of some breathing operants, that is, behaviors that may be reinforced:
● Aborted exhale
● Accessory muscle breathing
● Breath holding
● Deep/shallow breathing
● Disruptive thoughts
● Dysponesis
● Effortful breathing
● Fast/slow breathing
● Forced exhalation
● Gasping, sighing, coughing
● Intentional manipulations
● Interpretation of symptoms
● Mouth/nasal breathing
● Overbreathing
● Underbreathing
● Reverse breathing
● Self-talk
● Transition time
9

10. DYSFUNCTIONAL BREATHING
Dysfunctional breathing is defined as behavior that compromises physiology
and/or psychology, acutely and/or chronically.
The reconfiguration principles of physiology, i.e., learning principles, point to the most
fundamental, practical, and profound factors that account for:
(1) the far-reaching effects of dysfunctional breathing habits (e.g., deregulated plasma pH,
chronic contraction of muscles in the jaw), as well as for
(2) the surprising benefits of self-regulatory breathing habits (e.g., improved cerebral blood
flow for improved attention, learning, and performance, or muscle reeducation that
supports jaw realignment).
10

11. RESPIRATORY FITNESS
The fundamental objective
When breathing allows for reflex-regulated gas exchange, its external
respiratory function is serving its purpose.
Respiratory fitness is about reflex-regulated gas exchange based on:
● extracellular pH,
● extracellular partial pressure carbon dioxide (PCO2), and
● blood plasma PO2.
It is about moment to moment regulation of:
● extracellular pH,
● electrolyte balance,
● blood flow,
● hemoglobin chemistry, and
● kidney function.
Respiratory fitness is optimal when fundamental feedback reflex mechanisms are
permitted to serve their function.
11

12. COMPROMISED MECHANICS
Dysfunctional habits not only seriously compromise respiration, but may also
directly disturb physiology and psychology on many levels.
Breathing habits may be dysfunctional as a result of triggering:
● PHYSICAL CHANGES in local physiology
● SOMATIC CHANGES (muscles) and their associated effects
● AUTONOMIC CHANGES and their associated effects
● CENTRAL CHANGES (cerebral) and their effects on motivation, emotion, and cognition
12

13. COMPROMISED RESPIRATION
When external respiration is disturbed by breathing habits it may result in an unbalanced
extracellular acid-base chemistry and failure to meet metabolic requirements.
Respiratory fitness is vital to health and performance, and must be regulated despite the
breathing acrobatics of talking, emotional encounters, and professional challenges.
Respiratory fitness needs to be in place regardless of whether or not one is relaxed or
stressed, excited or bored, active or inactive, working or playing, focused or distracted.
Learned breathing mechanics that preempt basic brainstem respiratory reflexes and decouple
regulatory feedback mechanisms, constitute respiratory compromise.
The “respiratory chemical axis,” of breathing, i.e., acid-base regulation, needs to remain
relatively stable despite significant changes in breathing mechanics, e.g., changes in rate, that
may be serving parallel objectives.
13

14. MEDIATED CONSEQUENCES
The impact of dysfunctional breathing on physiology is far reaching.
Dysfunctional breathing habits can cause, trigger, exacerbate, and perpetuate symptoms
and deficits of all kinds , ones that typically go “unexplained” or are mistakenly attributed to
other causes, e.g., stress. From a learning perspective these breathing mediated outcomes
become behavioral consequences, rather than the effects of external factors.
When respiration is compromised as a consequence of breathing habits, it may have
profound immediate and long-term effects that trigger, exacerbate, perpetuate, and/or
cause a wide variety of emotional (anxiety, anger), cognitive (attention, learning), behavioral
(public speaking, test taking), and physical (pain, asthma) changes that may seriously impact
health and performance (Fried, 1987; Laffey & Kavanagh, 2002).
14

15. PHASES OF RESPIRATION
There are 3 phases of respiration, the physiology of each one being important
to the understanding of how breathing behaviors, habits and their patterns
may be dysfunctional, adaptive, or embracing.
External respiration: the breathing mechanics of gas exchange.
Internal respiration: the chemistry of moving gases to and from the cells
Cellular respiration: O2 utilization for synthesis of ATP molecules
ATP is adenosine triphosphate, the molecule broken down by cells for energy.
15

16. EXTERNAL RESPIRATION
is about the mechanics of breathing, moving gases (air) in and out of the lungs. Specifically, it
is about oxygen acquisition and proper carbon dioxide (CO2) allocation.
Retaining the right level of CO2 in the alveoli of the lungs is fundamental to good respiration;
the presence of CO2 is responsible for the regulation of acid-base balance. This is normally
regulated by brainstem reflex mechanisms.
Breathing mechanics include the following kinds of behavior: locus of breathing (diaphragm,
accessory muscles), rate (fast, slow), depth (deep, shallow), intake (nasal, mouth), transition
time of exhale to inhale (preempting the reflex), exhalation (aborted), inhalation (holding),
and rhythmicity (e.g., gasping, breath holding).
16

17. GAS EXCHANGE
Outgoing blood PULMONARY CAPILLARY Incoming blood
(Arterial levels) (Venous levels)
40 mmHg PaCO2
40 mmHg 46 mmHg PCO2
95 mmHg PaO2
102 mmHg 40 mmHg PO2
Diffusion
PAO2 ˃ PaO2 PAO2 = [PIO2 - 1.2 X PaCO2)
Differs 5 to 15 mmHg
because V-Q ˂ 1 (gravity effect) 40 mmHg 102 mmHg PA = alveolar gas
PACO2 PAO2 Pa = arterial gas
ET = End Tidal gas
PI = inspired gas (at trachea)
P = partial pressure
ALVEOLUS
PetCO2 (38 mmHg) PO2 (159 mmHg)
PIO2 (149 mmHg), diluted by PH2O
PCO2 (0.3 mmHg)
(paper bag, about 8 mmHg)
Reference: Martin, Lawrence All You Really Need to Know to Interpret Blood Gases . 1992. Lea & Fibiger. Philadelphia.
17

18. CELLULAR RESPIRATION
is the utilization of oxygen (O2) in mitochondria
for the synthesis of adenosine triphosphate (ATP),
molecules that cells ultimately break down for their energy.
STEP 1: Glycolysis (2 ATP)
STEP 2: The Krebs cycle (2 ATP)
STEP 3: Electron transport (34 ATP)
STEP 4: Chemiosmosis (oxidative phosphorylation)
The final result is: C6H12O6 (glucose) + 6O2
→ 6H2O + 6CO2 + 38ATP molecules
When there is insufficient oxygen, pyruvic acid accumulates during Step 1, which then
ferments to form lactic acid, and is then buffered with bicarbonate (HCO3
-) ions.; the
pH of body fluids are thus maintained. If not, lactic acidosis is the result, a form of
metabolic acidosis.
18

19. INTERNAL RESPIRATION
is about ensuring
(1) the transport of oxygen in the blood from the lungs to tissue cells,
(2) the transport of metabolic CO2 from tissue cells to the lungs, and
(3) excretion and reallocation of CO2 for acid-base balance regulation.
19

20. CHEMICAL AXIS OF BREATHING
pH = [HCO3
‾] ÷ PCO2
Central to understanding RESPIRATORY FITNESS is
the Henderson-Hasselbalch (H-H) equation,
which describes pH regulation in extracellular fluids.
Extracellular fluids include:
● blood plasma,
● interstitial fluid (between cells),
● lymph, and
● cerebrospinal fluid.
PCO2 is partial pressure carbon dioxide,
regulated by moment to moment breathing.
[HCO3
‾] is bicarbonate concentration,
regulated by the kidneys (8 hours -5 days)
20

21. CRITICAL pH VALUES
Normal plasma pH levels are 7.36 to 7.44 (7.4 the magic number)
When pH values drop below 7.36, acidemia is the consequence.
When values rise above 7.44, alkalemia is the consequence.
Although the changes between 7.1 and 7.7, for example, appears small,
in reality, [H+] goes from 80 to 20 nmol/l (7.4 = 40 nmol/l), a 4:1 change!
Plasma levels below 7.36 and above 7.44 can result in significant
physical symptoms, psychological changes, and behavioral deficits.
Plasma pH levels below 6.9 and above 7.8 are fatal.
Plasma pH shifts up or down as a function of changes in:
1. PCO2 (denominator of the H-H equation), and
2. bicarbonate concentration (numerator of the H-H equation).
Values of pH in other extracellular fluids are different. Interstitial fluids have lower
values than blood plasma. Intracellular pH is also lower than plasma pH.
21

22. PCO2
Denominator of the Equation
Arterial levels of PCO2, i.e., PaCO2,
must remain between 35 and 45 mmHg (or 4.7 and 6.0 kPa)
to keep plasma pH within its normal pH range of 7.36 to 7.44, slightly alkaline.
Respiratory acidosis (pH < 7.36)
is the result increased levels of PaCO2.
Respiratory alkalosis (pH > 7.44)
is the result of reduced levels of PCO2.

23. CRITICAL VALUES OF PCO2
Practically speaking, behavioral hypocapnia
is defined as ETCO2 readings below 35 mmHg,
as a result of learned dysfunctional habits:
above 45 mmHg: hypercapnia
35-45 mmHg (4.7-6.0 kPa): normal range (pH = 7.46 to 7.34)
30-35 mmHg: moderate to mild hypocapnia
25-30 mmHg: serious to moderate hypocapnia
20-25 mmHg: severe hypocapnia.
23

24. CHEMO-REGULATORY REFLEXES
Balancing the H-H equation is achieved through the presence of receptor sites in
(1) the brainstem, that are sensitive to interstitial pH and PCO2, and
(2) the arterial system (aorta and carotid arteries) that are sensitive to plasma pH and PCO2.
Changes in pH and PCO2 in both locations together drive the respiratory centers in the
brainstem, along with PO2 changes also detected at arterial receptor sites.
If pH is too low (< 7.35), or too high (>7.45), PaCO2 is reduced or increased
by altering breathing rate and depth (minute volume).
Many patients have learned breathing habits that preempt these reflexes, normally operated
through the diaphragm and external intercostal muscles, by aborting the exhale and
intentionally “taking” the breath with accessory muscles, e.g., posterior trapezius. These
habits are unconscious and happen involuntarily.
24

25. HYPOCAPNIA
is a PaCO2 deficit.
When PaCO2 is too low (below 35 mmHg),
with deeper and/or faster breathing,
the denominator of the H-H equation is smaller.
Thus, the extracellular pH rises (above 7.44)
with resulting respiratory alkalosis,
a condition identified as hypocapnia.
Hypocapnia that is a consequence of dysfunctional
breathing habits is known as behavioral hypocapnia.
Low CO2 levels may also be indicative of reflexive compensatory responses to metabolic
acidosis, such as the build up of lactic acidosis during anaerobic exercise, where lower
PaCO2 levels raise and help to normalize levels of pH. In this case low CO2 levels would not
be associated with a corresponding respiratory alkalosis.
25

26. BEHAVIORAL HYPOCAPNIA
is the result of learned overbreathing behavior.
Behavioral hypocapnia is the result of overbreathing behavior, “over” breathing because
excessive CO2 is excreted, resulting in excessively high levels of pH .
When overbreathing is a consequence of either learned dysfunctional breathing
mechanics, or is reinforced directly with powerful reinforcements (e.g., dissociation),
hypocapnia is behavioral, and hence the term behavioral hypocapnia.
Behavioral hypocapnia (respiratory alkalosis,)may have profound immediate and long-term
effects that may trigger, exacerbate, perpetuate, and/or cause a wide variety of symptoms
that may seriously impact health and performance:
● emotional (anxiety, anger),
● cognitive (attention, learning),
● behavioral (public speaking, test taking), and
● physical (pain, asthma) changes
26

27. HYPERCAPNIA
is excessive PaCO2.
When PaCO2 is too high (above 45 mmHg), with shallower and/or slower
breathing, extracellular pH falls (below 7.36) with resulting respiratory acidosis,
a condition identified as hypercapnia.
Behavioral hypercapnia is the consequence of underbreathing,
not ventilating off adequate CO2 by breathing too slowly and/or too shallow.
Behavioral hypercapnia is rare. Hyperinflation is the most likely cause.
When PCO2 is 35 to 45 mmHg, in a healthy person, extracellular pH is normal
(7.36-7.44), and is known as eucapnia.
27

28. EFFECTS OF HYPOCAPNIA
From: Laffey, J. & Kavanagh, B. Hypocapnia. New England Journal of Medicine. 2002.
“…extensive data from a spectrum of physiological systems indicate that hypocapnia has the potential to
propagate or initiate pathological processes. As a common aspect of many acute disorders, hypocapnia
may have a pathogenic role in the development of systemic diseases.”
“Increasing evidence suggests that hypocapnia appears to induce substantial adverse physiological and
medical effects.”
“Hypocapnia has been clearly linked to the development of arrhythmias, both in critically ill patients and in
patients with panic disorder.”
“…further lowering of the partial pressure of arterial CO2 - even for a short duration - such as during
anesthesia for cesarean section - may have serious adverse effects on the fetus.”
“Hypocapnia is a common finding in patients with sleep apnea and may be pathogenic.”
“The causative role of hypocapnia in postoperative cognitive dysfunction is underscored by the finding
that exposure to an elevated partial pressure of arterial carbon dioxide [i.e., normalizing CO2 levels]
during anesthesia appears to enhance postoperative neuropsychologic performance.”
NEJM article, Hypocapnia
28

29. SUMMARY QUOTATIONS
The effects on hypocapnia on physiology are impressive.
“Hypocapnia-induced vasospasm is responsible for reduced cerebral blood flow and neurological symptoms,
for reduced coronary blood flow and chest pain, for paresthesia of limbs, and circumoral pallor.”
Thomson, Adams, & Cowan, Clinical Acid-Base Balance, 1997
“Reducing arterial CO2-tension is one of most efficient ways to decrease cerebral blood flow, and hence
intracranial pressure. However, the cerebral vasoconstriction caused by hyperventilation may be so intense
that the limits of cerebral ischemia can be reached.”
de Deyne, C. S., 2001, Dept. of Anesthesia and Critical Care, Ziekenhuis Oost-Limburg. Genk, Belgium
“This disruption in the acid-base equilibrium triggers a chain of systematic reactions that have adverse
implications for musculoskeletal health, including increased muscle tension, muscle spasm, amplified
response to catecholamines, and muscle ischemia & hypoxia.”
Schleifer, Ley, and Spalding, Journal of Industrial Medicine, 2002
29

30. UNEXPLAINED SYMPTOMS
Learned breathing behaviors may play an important role in the appearance of
unexplained symptoms as well as their disappearance.
Learned overbreathing results in CO2 deficiency, behavioral hypocapnia, which may seriously
and immediately disturb acid-base balance. Its effects on body chemistry may mediate
changes labeled as “unexplained symptoms,” including misunderstood performance deficits
and “effects of stress,” all of which may be mistakenly attributed to other causes.
Overbreathing is an excellent example of how learned behavior may have an immense and
ongoing impact on multiple physiological systems. They may cause, trigger, exacerbate, and
perpetuate symptoms and deficits of all kinds:
● physical symptoms (e.g., asthma, fatigue, pain, hypertension),
● performance deficits (e.g., public speaking, test taking, carpal-tunnel),
● emotional reactivity (e.g., anger, anxiety, impatience),
● cognitive deficits (e.g., attention, learning, problem solving),
● psychological changes (e.g., personality shifts, self-esteem), and
● virtually every known symptom of stress, immediate and long-term.
30

31. Behavioral Hypocapnia
PHYSIOLOGICAL EFFECTS
Hemoglobin chemistry
● Red blood cell CO2 diminishes while alkalinity increases,
thereby increasing hemoglobin’s affinity for oxygen
and inhibiting its distribution to cells (Bohr Effect).
● The same red blood cell physiology restricts
the amount of nitric oxide (NO) released by hemoglobin,
resulting in significant vasoconstriction.
The net effect is reduced oxygen and glucose resources
for cells that require them.
31

32. Behavioral Hypocapnia
PHYSIOLOGICAL EFFECTS
Plasma alkalemia and low PCO2
● Calcium ions are exchanged for hydrogen ions in smooth muscle resulting in
vascular, gut, and bronchial constriction.
● Electrolyte shifts result in muscular calcium-magnesium imbalance.
● Increased pH in muscles increases their resting tension levels.
● Decreased PCO2 suppresses substance P-induced epithelium-dependent relaxation.
The net effect is reduced oxygen and glucose supply to cells that require them with
possible serious outcomes:
● Cerebral hypoglycemia
● Ischemia (localized anemia)
● Reversible brain lesion effects
32

33. Behavioral Hypocapnia
PHYSIOLOGICAL EFFECTS
Interstitial alkalemia and electrolytes
● Muscles: Calcium ions are exchanged for hydrogen ions
in smooth and skeletal muscle and set the stage for
muscle spasm, weakness, stiffness, and fatigue.
● Neurons: Sodium and potassium ions are exchanged
for hydrogen ions in neurons, for example, which
increases their excitability, contractility, and metabolism.
33

34. Behavioral Hypocapnia
PHYSIOLOGICAL EFFECTS
Intracellular acidemia
The resulting oxygen deficit combined with
increased cellular excitability, contractility, and metabolism
increases the likelihood of intracellular lactic acidosis
in active tissues, e.g., in neurons and muscles (tetany).
34

35. Behavioral Hypocapnia
PHYSIOLOGICAL EFFECTS
Inhibitory and excitatory brain centers
● Reduced oxygen and glucose supply disrupt inhibitory control centers
(e.g., in the limbic system), and depending on the context,
may trigger emotions, e.g., anger, anxiety, euphoria, and stress.
● Deactivating inhibitory and excitatory centers may result in
state changes (neurochemistry reconfigurations) that regulate
other response repertoires, including emotional, behavioral, and cognitive.
● Low cerebral PaCO2 levels may disinhibit the hypothalamus
to activate the pituitary-adrenal system and its associated hormones
(e.g., ACTH), resulting in stress symptoms, acute and chronic.
See article in Plos Medicine
35

36. Behavioral Hypocapnia
PHYSIOLOGICAL EFFECTS
Long term effects
Chronic effects include major losses of bicarbonate and sodium ions, electrolytes that are
excreted as a result of CO2 deficit in the nephrons of the kidney.
“The body maintains pH very closely. Even 7.45 or 7.5 over time may have significant
consequences. If proteins don’t fold correctly, membranes may not function properly. An
improperly folded protein is viewed by macrophages as foreign, and can initiate an immune
response which could be involved in everything from autoimmune disease to Alzheimer’s.”
Jan Newman, M.D.
36

37. Behavioral Hypocapnia
PHYSIOLOGICAL EFFECTS
Other Effects
● Dishabituation
● Antioxidant reduction
● Thrombosis (blood clotting)
● Myofacial tissue compromise
● Exacerbation of inflammation
● Red blood cell rigidity
● Extracellular sodium deficiency (hyponatremia)
● Extracellular potassium deficiency (hypokalemia)
37

38. Behavioral Hypocapnia
PHYSIOLOGICAL EFFECTS
Exacerbation of health issues and complaints
● Neurological : epilepsy
● Cognitive: learning disabilities, ADD, ADHD
● Emotional: anger, phobias, panic attack, anxiety, depression
● Psychological: trauma, PTSD, drug dependence
● Vascular: hypertension, migraine, ischemia, hypoglycemia
● Cardiovascular: angina, heart attack, arrhythmias, ECG abnormalities
● Efficacy of drugs: shifts in pH and electrolyte balance alter absorption
● Fitness issues: endurance, muscle strength, fatigue, altitude sickness
● Gastric: irritable bowel syndrome (IBS), non-ulcer dyspepsia
● Respiratory: asthma, emphysema, COPD
● Chronic pain: injury, disease, systemic inflammation
● Pregnancy: fetal health, premature birth, symptoms during pregnancy
● Neuromuscular: repetitive strain injury (RSI), headache, orthodontic
● Sleep disturbances: apnea
● Psychophysiological disorders: headache, chronic pain, hypertension
● Behavioral: performance issues, speech, singing, task challenges
● Unexplained conditions: fibromyalgia, chronic fatigue
38

39. Behavioral Hypocapnia
SYMPTOMS AND DEFICITS
that may be triggered, exacerbated, caused, or perpetuated by behaviorally mediated
physiological changes and typically and mistakenly attributed to other causes,
may include the following:
RESPIRATORY
● shortness of breath
● breathlessness,
● bronchial constriction and spasm
● airway resistance,
● reduced lung compliance
● asthma symptoms, e.g., wheeze
● unable to breathe deeply
● chest tightness, pressure, and pain
● inflammation
39

40. Behavioral Hypocapnia
SYMPTOMS AND DEFICITS
PERIPHERAL
● trembling
● twitching
● shivering
● sweatiness,
● coldness
● tingling
● numbness
40

41. Behavioral Hypocapnia
SYMPTOMS AND DEFICITS
CARDIOVASCULAR
● palpitations
● increased rate
● angina symptoms
● arrhythmias
● nonspecific pain
● ECG abnormalities
41

42. Behavioral Hypocapnia
SYMPTOMS AND DEFICITS
EMOTIONAL
● anxiety
● anger
● fear
● panic
● apprehension
● worry
● crying,
● low mood
● frustration
● performance anxiety
● phobia
IMPORTANT
Many, perhaps most, of these kinds of “symptoms and deficits” are learned responses
to the effects of hypocapnia, e.g., inability to focus or remember triggers anxiety,
frustration, or anger.
42

43. Behavioral Hypocapnia
SYMPTOMS AND DEFICITS
STRESS AND AUTONOMIC HYPER AROUSAL
● tenseness
● acute fatigue
● chronic fatigue
● effort syndrome
● weakness
● headache
● burnout
● anxiety
● muscle pain
Virtually most known acute and chronic symptom and deficit
can be triggered by respiratory compromise.
43

44. Behavioral Hypocapnia
SYMPTOMS AND DEFICITS
SENSORY
● blurred vision
● dry mouth
● dry skin
● sound seems distant
● reduced pain threshold
● Tinnitus
● numbness,
● tingling (hands, lips)
● dishabituation
44

45. Behavioral Hypocapnia
SYMPTOMS AND DEFICITS
CONSCIOUSNESS
● dizziness
● loss of balance
● fainting
● black-out
● confusion,
● disorientation
● disconnectedness
● hallucinations,
● traumatic memories
● low self-esteem
● personality shifts
IMPORTANT
State changes set the stage for learning new behaviors, a sense of self,
accessed only through becoming hypocapnic. Breathing may become
a gateway to different psychological postures.
45

46. Behavioral Hypocapnia
SYMPTOMS AND DEFICITS
COGNITIVE
● dishabituation
● attention deficit
● inability to think
● confusion
● disorientation
● poor memory
● learning deficits
● poor concentration
46

47. Effects of hypocapnia on the brain
Vasoconstriction leads to a 60% reduction of oxygen.
47

48. Behavioral Hypocapnia
SYMPTOMS AND DEFICITS
SKELETAL MUSCLES
● tetany
● hyperreflexia
● spasm
● weakness
● fatigue
● pain
● chest pain, pressure, discomfort
● difficult to swallow
● feelings of suffocation
48

49. Behavioral Hypocapnia
SYMPTOMS AND DEFICITS
SMOOTH MUSCLES
● Reduced cerebral blood flow
(approx. 4% per mmHg: 25% at 34 mmHg, 60% at 25 mmHg)
● Reduced cerebral blood volume
● Cerebral vasoconstriction
● Coronary vasoconstriction
● Gut smooth muscle constriction
● Reduced placental perfusion
● Bronchiole constriction
● Cerebral and myocardial hypoxia (O2 deficit)
49

50. Behavioral hypocapnia
SYMPTOMS AND DEFICITS
ABDOMINAL
● nausea
● cramping
● bloatedness
● exacerbation of sensitivities, disorders
50

51. Behavioral hypocapnia
SYMPTOMS AND DEFICITS
MOVEMENT
● coordination
● reaction time
● balance
● eye-hand coordination
● perceptual judgment
51

52. Behavioral hypocapnia
SYMPTOMS AND DEFICITS
VASCULAR
● hypertension
● migraine
● digital artery spasm
● compromised placental blood flow
● ischemia (tissue anemia)
● red blood cell rigidity, thrombosis
52

53. Hypocapnia: ischemia and brain damage
Laffey, J. G., & Kavanagh, B. P. Hypocapnia. New England Journal of Medicine (2002); 347(1): 43-53.
53

54. Behavioral hypocapnia
SYMPTOMS AND DEFICITS
PERFORMANCE
● sleep apnea
● anxiety
● rehearsal
● focus
● endurance
● altitude sickness
● muscle function
● fatigue
● pain
54

55. Behavioral hypocapnia
SYMPTOMS AND DEFICITS
SLEEP
“One of the mechanisms by which application of noninvasive positive airway pressure reduces
central sleep apnea is by increasing hemoglobin oxygen saturation and increasing the partial
pressure of arterial carbon dioxide toward or above the apneic threshold. In fact, central sleep
apnea is predicted by the presence of hypocapnia during waking hours. Thus, hypocapnia is a
common finding in patients with sleep apnea and may be pathogenic.”
Laffey, J. G., & Kavanagh, B. P. Hypocapnia. New England Journal of Medicine (2002); 347(1): 43-53.
“We conclude that when apnea occurs under conditions in which central PCO2 is well below the CO2
setpoint, subjects are at risk of developing dangerous hypoxemia due to absence of a hypoxic
ventilatory response.”
Corne, S., Webster, K., Younes, M. Hypoxic respiratory response during acute stable hypocapnia. American Journal
of Respiratory and Critical Care Medicine; 167.9 (May 1, 2003): 1193-9.
55

56. UNEXPLAINED SYMPTOMS
Learned breathing behaviors may play an important role in the appearance of
unexplained symptoms as well as their disappearance.
Learned overbreathing results in CO2 deficiency, behavioral hypocapnia, which may seriously
and immediately disturb acid-base balance. Its effects on body chemistry may mediate
changes labeled as “unexplained symptoms,” including misunderstood performance deficits
and “effects of stress,” all of which may be mistakenly attributed to other causes.
Overbreathing is an excellent example of how learned behavior may have an immense and
ongoing impact on multiple physiological systems. They may cause, trigger, exacerbate, and
perpetuate symptoms and deficits of all kinds:
● physical symptoms (e.g., asthma, fatigue, pain, hypertension),
● performance deficits (e.g., public speaking, test taking, carpal-tunnel),
● emotional reactivity (e.g., anger, anxiety, impatience),
● cognitive deficits (e.g., attention, learning, problem solving),
● psychological changes (e.g., personality shifts, self-esteem), and
● virtually every known symptom of stress, immediate and long-term.
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57. MECHANICS AND CHEMISTRY
Breathing is acrobatic. It fits all occasions. And, if it is adaptive, it serves
fundamental respiration most of the time.
Good respiratory fitness is optimal distribution of oxygen and adaptive pH regulation, both
of which go hand in hand. Good breathing maintains a stable “chemical axis” in accordance
with the H-H equation that describes extracellular pH regulation.
As a result of very specific learning, dictated by unique learning histories, breathing
behaviors and patterns may change dramatically and immediately as a function of physical
and social circumstances along with what a person may be doing, thinking, and feeling.
Nevertheless, maintaining a stable respiratory chemical axis (pH regulation) is vital to
health and performance, and must be regulated despite the breathing acrobatics of talking,
emotional encounters, and professional challenges.
Learned dysfunctional breathing may seriously compromise respiratory function. It may
disturb fundamental biochemistry and physiology that touches all other physiological
systems, and may do so both profoundly and immediately.
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58. ASSESSMENT
Applied Behavior Analysis
Behavior analysis is serious detective work, a client-practitioner partnership in
the exploration of physiology, behavior, and experience.
Practitioners and clients work together to uncover the specific learning histories of
maladaptive breathing habits, including the specific behaviors learned and their triggers,
their reinforcements, and their effects.
Clients learn about how and why they breathe the way they do, and how unconscious habits
may be influencing their health and performance. These are the objectives of applied
behavior analysis.
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59. CAPNOGRAPHY
Capnography is instrumentation used in surgery, critical care,
emergency medicine, and behavioral assessment.
Capnography provides for real time monitoring of alveolar PCO2; that is, measurement of the
amount of CO2 retained in the alveoli, not the amount exhaled.
Capnographs (capnometers) provide for a continuous measurement of PCO2 while breathing, both
during the inhale and the exhale. During the inhale it reads effectively “zero,” as there is a very
small amount of CO2 in atmospheric air (0.3 mmHg), as compared to a total pressure of 760 mmHg.
During the exhale, PCO2 rises sharply in the lungs, continues to rise very slowly during the transition
from exhale to inhale (the alveolar plateau), and eventually reaches a peak value immediately prior
to the next inhale. This peak value can be thought of as the “End of the Tide of air, and is known as
End Tidal PCO2, written PetCO2, or ETCO2.
This waveform is known as a capnogram.
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60. THE CAPNOGRAM
The continuous and real-time presentation of waveform data permits
observation of air flow, including breath-holding, gasping, spasm, sighing,
breathing rate, aborted exhalation, and rhythmicity.
From Levitsky, 2007
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61. PCO2 MEASUREMENT
Actual quantities of carbon dioxide generated by the body vary considerably based on
metabolism, e.g., meditation vs. exercise, although the PaCO2 values required for
maintaining acid-base balance (35-45 mmHg) remain the same.
At rest, for example, only about 15 percent of the CO2 arriving in the lungs is excreted; the
balance is reallocated to systemic circulation. While doing exercise, of course, the PCO2
arriving in the lungs is radically increased.
Capnograph instrumentation
does NOT indicate how much CO2 is being exhaled.
Capnographs provide average values of alveolar PCO2 (PACO2),
that is, the end-tidal reading (PetCO2) at the end of the exhale.
If the exhale is aborted, PetCO2 will read lower than PACO2.
Capnographs provide for continuous measurement of PCO2 (raw wave form),
and allow observation of air flow, e.g., gasping, breath holding, aborted exhales.
PetCO2 approximates arterial PCO2 (PaCO2)
because PACO2 is equivalent to PaCO2 (although slightly lower).
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62. AIR FLOW: GASPING
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63. AIR FLOW: SPASM
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64. AIR FLOW: STRUGGLE
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65. CLIENT-CENTERED SERVICES
Breathing learning services are client-centered.
What does this mean?
● Practitioners are guides, coaches, consultants who assist in learning.
● Breathing learning services do not involve diagnosis or treatment.
● Clients subscribe to, or register for, learning programs, not therapy sessions.
● Clients and practitioners work together in a partnership.
● Clients do most of the work, and they do it the field, at home and at work.
● Emphasis is on what clients learn, not what practitioners do.
The basic skills required are communication skills, including interviewing, listening,
counseling, and teaching. Required knowledge includes basic physiology, basic
psychology, and a background working with the relevant client population, such as
clients suffering with asthma, heart conditions, trauma, learning problems, or
performance issues.
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