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Litchfield spreecast ppt slides

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Litchfield spreecast ppt slides

  1. 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. 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. 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. 4. OBJECTIVE Applied Breathing Sciences Clients learn new breathing habits, and related behaviors, that are consistent with healthy physiology and psychology. 4
  5. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 40. Behavioral Hypocapnia SYMPTOMS AND DEFICITS PERIPHERAL ● trembling ● twitching ● shivering ● sweatiness, ● coldness ● tingling ● numbness 40
  41. 41. Behavioral Hypocapnia SYMPTOMS AND DEFICITS CARDIOVASCULAR ● palpitations ● increased rate ● angina symptoms ● arrhythmias ● nonspecific pain ● ECG abnormalities 41
  42. 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. 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. 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. 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. 46. Behavioral Hypocapnia SYMPTOMS AND DEFICITS COGNITIVE ● dishabituation ● attention deficit ● inability to think ● confusion ● disorientation ● poor memory ● learning deficits ● poor concentration 46
  47. 47. Effects of hypocapnia on the brain Vasoconstriction leads to a 60% reduction of oxygen. 47
  48. 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. 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. 50. Behavioral hypocapnia SYMPTOMS AND DEFICITS ABDOMINAL ● nausea ● cramping ● bloatedness ● exacerbation of sensitivities, disorders 50
  51. 51. Behavioral hypocapnia SYMPTOMS AND DEFICITS MOVEMENT ● coordination ● reaction time ● balance ● eye-hand coordination ● perceptual judgment 51
  52. 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. 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. 54. Behavioral hypocapnia SYMPTOMS AND DEFICITS PERFORMANCE ● sleep apnea ● anxiety ● rehearsal ● focus ● endurance ● altitude sickness ● muscle function ● fatigue ● pain 54
  55. 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. 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. 56
  57. 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. 57
  58. 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. 58
  59. 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. 59
  60. 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 60
  61. 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). 61
  62. 62. AIR FLOW: GASPING 62
  63. 63. AIR FLOW: SPASM 63
  64. 64. AIR FLOW: STRUGGLE 64
  65. 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. 65

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