Dysfunctional breathing context, causes and contributing-spree cast may 2013
1. Dysfunctional Breathing -Context,
Causes and Contributing Factors
Dr. Rosalba Courtney ND, DO, PhD
Lecture for Airway and Facial Development
Collaborative- May 2013
2. Functional Breathing is Adaptive,
Appropriate, Responsive
Functional breathing is breathing that performs and adapts its
various functions to quickly and appropriately meet the changing
needs of the individual and changes in the internal and external
environment.
It adapts appropriately to rest and activity.2Rosalba Courtney 2013
3. Functional breathing- efficiently maintains
the functions of breathing
• Primary
– Biochemical- Optimise O2 and CO2, pH regulation and
metabolism.
– Biomechanical- Optimise neuromuscular respiratory pump.
• Secondary
– motor control and postural stability
– regulation of homeostatic e.g. cardiorespiratory oscillations via
cardiopulmonary coupling
– regulation of ANS and modulation of vagal activity
– self-regulation of stress and emotion.
– psycho-spiritual functions
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4. Functional breathing is the most
efficient breathing for the conditions
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5. What is Dysfunctional Breathing
• Dysfunctional breathing is not adaptive, responsive or
appropriate.
• Dysfunctional breathing is not the most efficient breathing for
the conditions
Dysfunctional breathing results in disturbance
or inefficiency of the primary or secondary
functions of breathing.
Dysfunctional Breathing contributes to
symptoms and pathology.
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6. Dysfunctional Breathing has several dimensions
Biochemical
• CO2
• pH
• O2
• Hyperventilation
Biomechanical
• Paradoxical
• Thoracic Breathing
• Irregular
• Inefficient/Weakness, Co-
ordination
Psycho-
physiological
• Symptoms
• Perception
• Stress
• Anxiety/Fear
• Depression
Rhythms and
Oscillations
Stability
Homeostatis
Cardiorespiratory
Control and
Efficiency
Autonomic
Nervous System
Rosalba Courtney 2013
6
7. Separate dimensions of DB- overlap
but not completely
Neuro Muscular-
Breathing Pattern
and Habits
-
Biochemical-
CO2, O2, pH
Breathing
Symptoms
Psychophysiological-
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8. 8Rosalba Courtney 2013
COURTNEY, R.,
GREENWOOD, K. &
COHEN, M. 2011.
Relationships
between measures
of dysfunctional
breathing in a
population with
concerns about their
breathing. Journal of
Bodywork and
Movement
Therapies, 15, 24-
34.
9. - target the breathing therapy to the individual.
-consider underlying factors and treat causes if possible
- consider key aspects of breathing functionality
- evaluate and measure progress
Rosalba Courtney 2011
To be most effective breathing therapy should focus on
the patient, their specific breathing dysfunction and its
causes
10. Breathing responds to many conditions.
Breathing functionality depends on context.
BREATHING
Psychophysiology
Muscular and
Skeletal
Disease processes
Homeostasis
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11. Breathing patterns that seem dysfunctional can be
appropriate in certain circumstances.
LRC/ABD URC
Animation adapted from Lasovetskaya 2008
Relaxed
Configuration-
Natural at rest, in relaxed
state for healthy individual
Active
Configuration-
natural tendency for
increased respiratory
drive, increased rate or
volume of breathing,
especially if sudden.
11
Rosalba Courtney 2013
12. Thoracic Breathing- URC breathing
Dysfunctional when habitual and thoracic
dominance persists at rest.
i.e. active configuration during relaxation
In some cases can preserve diaphragm
length and curvature better because
maintains abdominal tone. So can be
appropriate in some COPD patients etc.
12Rosalba Courtney 2013
13. Mouth Breathing – a serious
dysfunction with many consequences-
structural, postural and health
15. Children with long standing nasal obstruction have
significantly lower oxygen.
Parameter Normal
Control
Obstructed-
Pre surgery
Obstructed-
Post surgery
Oxygen
Saturation
(SpO2)- Range
84-94% 87-97%
Oxygen
Saturation
(SpO2)- Mean
96.0% (1.4) 89.4% (3.0) 93.5%(3.0)
Arterial
Oxygen
(PaO2)-Range
57-84mmHg 67-102mmHg
Arterial
Oxygen
(PaO2)-Mean
90.33
(6.85)mmHg
70.93
(6.07)mmHg
87.83
(12.13)mmHg
KHALIFA, M. S., KAMEL, R. H., ZIKRY, M. A. & KANDIL, T. M. 1991. Effect of enlarged
adenoids on arterial blood gases in children. Journal of Laryngology and Otology, 105,
436-438
16. Mouth breathing in a child with
obstructed airways
Functional-Situation 1
Child closes their
mouth and O2 levels
drop.
However mouth
breathing has many
negative consequences
so new problems arise.
Dysfunctional- Situation 2
Child closes their mouth
and O2 levels rise.
17. Children with long standing nasal obstruction have
slightly lower CO2 levels on average (some in
hyperventilation range- not always).
Parameter Normal
Control
Obstructed-
Pre surgery
Obstructed-
Post surgery
Arterial CO2
(PaCO2)-
Range
32-44mmHg 33-44mmHg
Arterial CO2
(PaCO2)-Mean
39.17 (1.64)
mmHg
38.57
(3.54)mmHg
37.6
(3.14)mmHg
KHALIFA, M. S., KAMEL, R. H., ZIKRY, M. A. & KANDIL, T. M. 1991. Effect of enlarged
adenoids on arterial blood gases in children. Journal of Laryngology and Otology, 105,
436-438
18. Hypoxia usually decreases CO2
tolerance.
Hypoxia increases the sensitivity
and ventilatory recruitment
threshold of the peripheral
chemoreflex response to CO2.
Hyperventilation to some extent be an
adaptive response to hypoxia. This has a cost
and negative consequences but loss of this
response may also lead to problems. (see
following study).
19. FREGOSI, R. F., QUAN, S. F., JACKSON, A. C., KAEMINGK, K. L., MORGAN, W. J.,
GOODWIN, J. L., REEDER, J. C., CABRERA, R. K. & ANTONIO, E. 2004. Ventilatory
drive and the apnea-hypopnea index in six-to-twelve year old children. BMC Pulm
Med. , 4.
High CO2 and low ventilatory drive
correlated with more severe sleep apnea
Fifty children, 6 to 12 years of age were studied
Asleep-Polysomnogram to compute the OAHI.
Awake- Measured ventilatory drive – normoxia, isocapnic hypoxia,hyperoxic hypercapnia
CONCLUSIONS:
In awake children the OAHI correlates inversely with the hypoxic ventilatory drive and
positively with the resting PETCO2.
Reduced hypoxic ventilatory drive and resting CO2 retention are associated with sleep-
disordered breathing in 6-12 year old children
.
20. Context of hyperventilation and mouth
breathing should guide treatment
decisions
Hyperventilation and Mouth Breathing may
be semi- functional adaptations to
obstruction and hypoxia.
They may be difficult to treat until we raise
oxygen levels and increase airway size.
21. Maladaptive Respiratory Plasticity as a
Cause of Dysfunctional Breathing
BAKER, T. L., FULLER, D. D., ZABKA, A. G. & MITCHELL, G. S. 2001. Respiratory
plasticity: differential actions of continuous and episodic hypoxia and
hypercapnia. Respiratory Physiology, 129, 25-35.
Long Term Facilitation (LTF)- alters
neuroplasticity of respiratory motor
control.
Hypoxia
Hypercapnia
22. Hypoxia, Hypercapnia can also
stimulate adaptive changes in
neuroplasticity of breathing.
• Activate Long Term Facilitation (LTF)
– Increase chemosensitivity
– Active airway dilator muscles via vagus and
hypoglossal nerve.
LTF can be adaptive and protective in situations like
sleep apnoea or maladaptive if it results in
inappropriate breathing.
23. Stress and Excess Allostatic Load is an important source of dysfunctional
breathing.
Modified from McKewen 1998
Perceived Stress-threat,
helplessness, vigilance
Behavioural
Response
Physiological
Response
Individual differences
Allostasis
Adaptation
Allostatic Load
Environmental
Stressors
Major Life Events Trauma Abuse
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24. Dysfunctional breathing evidence of a general
instability of the homeostatic brain.
Entrophy of
Respiration
Cardio-
respiratory
coupling and
HRV
Balance system
abnormalities
Respiration, cardiovascular homeostasis are interrelated and disruptions in one often
accompanied by others
PERNA, G., CALDIROLA, D. & BELLODI, L.
2004. Panic disorder: from respiration to
the homeostatic brain. Acta
Neuropsychiatrica, 16, 57-67.
24Rosalba Courtney 2013
Hypothesis-
Abnormal
Function of the
Homeostatic
Brain
25. Babies especially responsive to
respiratory neuroplasticity in sensitive
development periods
-hypoxia
-hypercapnia
-stress
-injury
-trauma
Altered mature
respiratory
control
Marcus et al. Developmental Aspects of the Upper Airway-Report from an NHLBI
Workshop, March 5–6, 2009. Proc Am Thorac Soc. , 15, 6.
26. Birth Trauma, structural
dysfunction and breathing.
“all cases of persistent C0 –
C1 compression are
accompanied by a
dysfunction of the
sphenoid-vomer
articulation. This pattern in
its pure form is mainly
inherent to children and is
usually connected with a
birth trauma”
From ……
Dr Larissa Lasovetskaya
2008
28. Symptoms- hyperinflation, short flat
diaphragm, rib cage stiffness and
neuromechanical uncoupling
28Rosalba Courtney 2013
•High dyspnoea
•Unsatisfied respiration
•Cant take a deep or satisfying
breath
•Rib cage cant expand
Dysfunctional Breathing
•Mouth Breathing
•Hyperventilation
•Breathing Pattern
29. Disproportionate and unexplained nasal
obstruction explained by dysfunctional
breathing (HV and BPD)
BARTLEY, J. 2006. Nasal congestion and HVS. Am J Rhinology, 19,
607-11.
14 patients with unexplained ongoing
nasal congestion after surgery and
medication.
Breathing- 3 patients underwent
capnometry and CO2 <35mmHg, all had
tachypnoea, upper thoracic bpd , 12 high
NQ score,
30. Does Hyperventilation contribute to
obstruction and mouth breathing?
YES
• Hyperventilation increases
nasal resistance.
Dallimore,, 1977Acta Otolaryngol, 84, 416-
421.
• Raising CO2 can decrease
nasal resistance and treat
seasonal rhinitis .
Casale, 2008.J Allergy Clin Immunol.
121, 105-109.
• There is a linear relationship.
Mertz, 1984. Otolaryngol Head Neck
Surg., 92, 302-307.
Is Hyperventilation primary cause
obstruction and mouth breathing?
NO
• Large amount of
epidemiological and
experimental evidence
showing that the cause
of obstructed airways
and respiratory allergy
is related to recent
changes in the
environment, diet and
state of the modern
human microbiome.
31. Causes of DB in children-increased nasal
resistance and obstruction of upper airway
• “mouth breathing happens whenever the body senses that nasal resistance is too high”
- Food and
airborne allergy
-Hypertrophy
lymphoid tissue
-nasal changes venous
engorgement, polyps
32. Is Hyperventilation the main cause of
allergy, inflammation, asthma, sleep
apnea, 150 other diseases .... NO
Is Hypocapnia important...YES
33. Role of CO2 in the Body
CO2
Mild Broncho/Vessel Dilator pH Buffering
Activity of Enzymes
and Mediators
34. Role of CO2 in the Body
CO2
Mild Broncho/Vessel Dilator pH Buffering
Activity of Enzymes
and Mediators
A Substrate for the Synthesis of
Essential Aminoacids and Enzymes
35. Low CO2
- Bronchocontriction
- Blood supply to the
brain
- Blood supply to the
tissues
Changes in
pH
Changes in activity
of Enzymes
Deficit in essential
aminoacids,
neuromodulators and
Neurotransmitters
Impairment
in Oxygen
utilisation
Decrease in buffering
capacity, wash out
essential cations:
- Calcium,
- Magnesium,
- Zinc,
- Potassium,
- Sodium
Overexcitability
of Nervous
system
36. History Of Hyperventilation Syndrome
Pre-
1980’s
After
1980’s
1990’s
NOW
HV back on the
radar-better
diagnostics.
Hypocapnia
found to
moderate
symptoms in
asthma, panic
disorder.
HVS not back.
Accepted diagnosis
patients with
anxiety, disturbed
breathing and
unexplained
“psychosomatic”
symptoms .
Argued to be
common, yet
infrequently
recognized
(Lum 1975; Lum
1976; Magarian
1982).
Increasing
doubts about
the specific
role of CO2 in
symptoms of
HVS and
HVPT
Recommended
that the term
hyperventilation
syndrome be
discontinued
(Hornsveld 1997)
Careers ruined.
Scientists
would not
touch it.
Labs stopped
researching
hypocapnia.
37. Hyperventilation Syndrome-Changing
Definition
4th International Symposium on
Psychophysiology in Southampton in 1984
3rd International Conference of Respiratory
Psychophysiology Nijmegen, 1997
• “Hyperventilation syndrome
is a syndrome characterized
by a variety of somatic
symptoms induced by a
physiologically
inappropriate
hyperventilation and usually
produced in whole or in part
by voluntary
hyperventilation” p287, (Howell
1990).
• Hyperventilation Syndrome
is “ a dysregulation of
ventilation, causing
hypocapnia, in the absence
of somatic causes for
hyperventilation, with
symptoms not necessarily
linked to hypocapnia” p73
(Molema and Folgering 1997).
38. There has been a huge increase in allergic,
inflammatory and immune diseases in last 50-
60 yrs in developed world.
One in three children has allergies. This
accounts for about a 400% increase in
the last 30-40 years.
It is predicted* this will increase to 1 in
2 children by the year 2015.
Asthma has increased by about 300%
*Global Allergy and Asthma European Network
40. Causes of increased allergy, asthma and
immune dysfunction are environmental.
• International study of asthma and allergy in childhood
(ISAAC) a study of 798,685 childen aged 13-14 years
from 97 countries and 388,811 children aged 6-7 yrs
from 61 countries.
• Conclusion-
The major differences between populations due to
environmental factors.
• ISAAC 1998. Worldwide variations in the prevalence of
asthma symptoms: the International Study of Asthma
and Allergies in Childhood (ISAAC). European Respiratory
Journal, 12, 315-335.
41. Differences in Asthma and Allergy Levels between
East and West Germany at Time of Re-Unification
• Allergy considerably
more frequent in West
German children than in
their peers in East
Germany (36.7% versus
18.2%; )
• Asthma and hay fever
also significantly higher
in West Germany than
East Germany (5.9%
versus 3.9%).
The Berlin Wall -1946-1989
VON MUTIUS, et al 1994. Prevalence of asthma and atopy in two areas of West
and East Germany. American Journal of Respiratory and Critical Care
Medicine, 149, 358-64.
42. Studies point to several environmental factors
that influence allergy and asthma
• Urban vs Rural
Living
• Prosperity
• Exposure to Animals
• Changes in Diet
• Microbial Diversity
in Water, Food, Air
etc.
43. MORGAN et al. 2013. Biodiversity and functional genomics in the human microbiome.
Trends in Genetics, 26, 51-58.
44. Old Friends Theory- Immune dysregulation
in modern urban humans related to
missing organisms we co-evolved with .
.
ROOK, G. A. 2007. The hygiene hypothesis and the increasing prevalence of chronic
inflammatory disorders. Trans R Soc Trop Med Hyg, 101, 1072-4.
The 'Hygiene' or 'Old Friends' hypothesis suggests that increases in chronic
inflammatory disorders (allergies, inflammatory bowel disease and autoimmunity)
in developed countries are partly attributable to diminishing exposure to
organisms that were part of mammalian evolutionary history. Crucial organisms,
including helminths and saprophytic mycobacteria, are recognised by the innate
immune system as harmless or, in the case of helminths, as organisms that once
established must be tolerated. This recognition then triggers development of
regulatory dendritic cells that drive regulatory T-cell responses to the 'Old Friends'
themselves and to simultaneously processed 'forbidden' target antigens of the
chronic inflammatory disorders.
45. Many Old Friends Live in our Gut-
•Intestinal microflora is major
external driving force in the
maturation of the immune system .
•Prerequisite for development of
normal tolerance to allergens.
•Microflora differs between
healthy and allergic infants.
•Microflora differs in countries
with high and low prevalence of
allergies.
Bjorksten “Evidence of probiotics in prevention of allergy and asthma”
Curr Drug Targets Inflamm Allergy 2005;4(5):599-604
46. Farm milk protects against asthma
whether or not you live on a farm
In a study of 14,893 children aged 5 to
13, drinking raw milk was the strongest
factor in reducing the risk of asthma
and allergy, whether the children lived
on a farm or not.
Inverse Association of farm milk consumption with asthma and allergy, in rural
and suburban populations across Europe” 2007 Waser M., Michels et al.Clinical
and Experimental Allergy , 2007,37 (5): 661-670
I
47. Why ? –Effect of farm milk on gut
•Presence of compounds like
Lactoferrin boosts immunity
•Raw Milk is perfect medium
for human probiotic organisms
48. The gut, the lungs and the immune system
•Gut interacts with intestinal bacteria
• Beneficial Bacteria (BB) lead to improved
gut barrier and immune stimulation.
•Good gut barrier and BB produces
tolerance to allergens.
•Microbial environment and exposure to
BB in infancy affects development of
asthma and allergy.
Bjorksten B.,“Effects of intestinal microflora and the
environment oon the development of asthma and allergy”
(2004) Springer Seminars Immunopath. 25(3-4):257-70
49. Clinical results improve the closer you are to
fundamental causes.
Symptoms and
Behaviours
Growth and Development
Microbiome, inflammation, allergy, immune
Breathing Dysfunction
Structural Changes
Social, Environment, Food, Stress
50. Thank You
Dr. Rosalba Courtney
breathandbody@optusnet.com.au
www.breathandbody.com.au
61-2-99183460
facebook.com/RosalbaCourtneysBreathAnd
BodyHealth
Editor's Notes
“if we observe successful people we can often see that they display a wonderful flexibility in reacting, in constantly changing from activity to rest. They have flexible breathing or functional breathing” Elsa Gindler
The term ‘dysfunctional breathing’ (DB) has been used increasingly over the last decade, particularly by those involved in breathing therapies (Thomas 2003; Hagman, Janson et al. 2008; Stanton, Vaughn et al. 2008). Its use has increased after doubts about the presence of hypocapnia in patients with the hyperventilation syndrome made the use of this term unacceptable (Dixhoorn 1997; Hornsveld 1997). At times it seems that the term dysfunctional breathing has been used as a proxy for the term hyperventilation syndrome, given that the main criteria for diagnosing DB has been the Nijmegen Questionnaire (Thomas, McKinley et al. 2001; Thomas, McKinley et al. 2005), a questionnaire that was originally validated for hyperventilation (Dixhoorn and Duivenvoorden 1985). However, at other times the term dysfunctional breathing has been used to refer exclusively to breathing pattern dysfunction (Prys-Picard and Niven 2008) or when unusual and disordered breathing patterns exist in combination with medically unexplained symptoms and anxiety (Hagman, Janson et al. 2008; Stanton, Vaughn et al. 2008).
Biochemical – relates to levels of O2, Co2, and pH. Most common biochemical dysfunction is hyperventilation but some people also hypoventilate. Biomechanical- relates to breathing pattern dysfunction e.g. thoracic breathing, paradoxical breathing, excessively irregular breathing or where there is weakness and poor co-ordination in patterns of muscle use during breathing. Psychophysiological-
Breathing is responsive to many factors e.g. psychological, neurological, structural and pathological Breathing that appears dysfunctional may simply be the body’s best attempt at adapting to a particular set of circumstances. To effectively correct any aspect of dysfunctional breathing it is important to take into account the context in which they occur, their causes and contributing factors.
In a small percentage of these children asking them to close their mouth will reduce oxygen levels. In these children mouth breathing is a ‘somewhat’ functional adaptation to obstructed airways. While we do want to train all children to stop mouth breathing in this particular group it is not the first step. The first step is to somehow increase the size of the airway. In the rest asking them to close their mouth causes O2 levels to rise. In these cases mouth breathing is a dysfunctional adaptation. One of the first priorities in these children is to train them not to mouth breath. In the majority of children asking them to close their mouths, does not create any immediate change in oxygen levels. However because of the many negative effects of mouth breathing ( which I don’t have time to go through in this talk or just a quick slide), we still need to train them not to mouth breathe.
Maladaptive Respiratory Neuroplasticity.Respiratory plasticity is defined as a persistent change in the neural control system based on prior experience.Plasticity may involve structural and/or functional alterations (most commonly both) and can arise from multiple cellular/synaptic mechanisms at different sites in the respiratory control system. Respiratory plasticity can be induced by hypoxia, hypercapnia, exercise, injury, stress, and pharmacological interventions or conditioning and occurs during development as well as in adults. Hypoxemia and hypercapnia can lead to a habitual change of breathing pattern because of the process know as Long Term Facilitation (LTF), a process in which alters neuroplasticity of respiratory motor control.
Breathing modulates arousal, restores homeostasis.“The biological purpose of the aroused state is to allow an organism to ‘cope’ physiologically, behaviorally and emotionally with specific environmental demands. Arousal must be followed by a period of relaxation for homeostasis to be restored” (Sterling and Eyer 1988). p94
Babies especially responsive to respiratory neuroplasticity- Developmental plasticity is induced by experiences (e.g., altered respiratory gases) during sensitive developmental periods, thereby altering mature respiratory control. The same experience later in life has little or no effect. In adults, neuromodulation plays a prominent role in several forms of respiratory plasticity. For example, serotonergic modulation is thought to initiate and/or maintain respiratory plasticity following intermittent hypoxia, repeated hypercapnic exercise, spinal sensory denervation, spinal cord injury, and at least some conditioned reflexes. Some factors that are thought to contribute to maladaptive plasticity include- Intermittent hypoxia, supplemental oxygen, maternal separation, stress, malnutrition (Marcus et al., 2009).Marcus et al. Developmental Aspects of the Upper Airway-Report from an NHLBI Workshop, March 5–6, 2009. Proc Am Thorac Soc. , 15, 6.
Birth TraumaAccording to Dr. LassissaLasovetskyas of St Petersburg College of Osteopathic Medicine- studies of posture and skeletal motion done on more than 1000 children comparing those with normal and dysfunctional breathing patterns revealed a consistent pattern of C0-C1 dysfunction, sphenoid and vomer fixation. She and her colleagues believe that this pattern in its pure form is mainly inherent to children and is usually connected with a birth trauma. “The first movement performed by the baby during labor is flexion. It is the only kind of engagement, which allows the head to enter the birth canal with its minimal size. But there are occasions, when this kind of engagement does not happen, and instead the head is shifted forward with elements of extension. After birth it will manifest in marked C0 - C1 compression and compensatory hyper-mobility in C1 – C2 segment in flexion”.Dr. Lasovetskaya describing the children with sniffing type breathing “In 100% of cases osteopathic examination demonstrated C0 – C1 compression, absence of nodding movement at this level, translation of the whole segment anteriorly, compensatory hyper-mobility in C1 – C2 segment in flexion. Nearly in half of these children these lesions were combined with intraosseous compression of the occiput”.
The sensation of dyspnea or breathlessness is strongly influenced by how the brain interprets and responds to the activity of the respiratory muscles, the tension in the chest wall and the shape, length and strength of the diaphragm. Dyspnea increases and reaches distressing levels when the respiratory motor output does not result in the expected response by the respiratory muscles and the chest wall.
People with this sort of problem can be recognised by disproportionate or unexplained dyspnea, sighing respiration, a vertical breathing pattern, symptoms of “unsatisfied respiration”. “I cannot take a deep or satisfying breath”. “My ribcage feels stuck and cant expand”. They might also continue mouth breathing even though the airways are adequate.
Abstract:Background: This article evaluates the prevalence of hyperventilation syndrome (HVS) in patients who continue to complain of ongoing nasal congestion, despite an apparently adequate surgical result and appropriate medical management.Methods: Prospective case series of 14 patients from June 2002 to October 2003 was performed. Patients, who presented complaining of nasal congestion after previous nasal surgery and who appeared to have an adequate nasal airway with no evidence of nasal valve collapse, were evaluated for HVS. When appropriate, nasal steroids and oral antihistamines also had been tested without success. Three patients had end-tidal PCO2 levels measured and five patients underwent breathing reeducation.Results: All patients had an elevated respiratory rate (>18 breaths/minute) with an upper thoracic breathing pattern. Twelve of the 14 patients complaining of nasal obstruction had an elevated Nijmegen score indicative of HVS. An average number of 2.5 procedures had been performed on each patient. End-tidal PCO2 levels were ≤35 mmHg in the three patients who had expired PCO2 levels measured. Breathing retraining was successful in correcting the nasal congestion in two of five patients.Conclusion: HVS should be included in the differential diagnosis of patients presenting with nasal congestion, particularly after failed nasal surgery. One possible explanation is increased nasal resistance secondary to low arterial PCO2 levels. Another possible explanation is reduced alaenasae muscle activity secondary to the reduced activity of serotonin-containing raphe neurons. Additional surgery may not necessarily be the answer in HVS patients complaining of nasal congestion.
Yes. It is a contributing factor. Several studies showing that mouth breathers (those milder obstruction) can tend to lower CO2.Hyperventilation is linearly related to increased nasal resistance so its reasonable to assume it is a contributing factor. Nasal resistance decreases linearly as expired CO2 levels and exercise levels increase, minute ventilation increases linearly as expired CO2 levels and exercise levels increase, and nasal resistance varies inversely with minute ventilation during both hypercapnia and exercise. The constant relationship between nasal resistance and minute ventilation during hypercapnia and exercise suggests that nasal resistance is regulated by the respiratory center to match the level of respiratory demand. (Mertz and McCaffrey, 1984) Raising CO2 can decrease nasal resistance and treat seasonal rhinitis(Casale et al., 2008). Hyperventilation increases nasal resistance (Dallimore and Eccles, 1977)
Before the 1980s, Hyperventilation Syndrome (HVS) was a generally accepted diagnosis for patients with anxiety, disturbed breathing and unexplained “psychosomatic” symptoms and was argued to be common, yet infrequently recognized (Lum 1975; Lum 1976; Magarian 1982). Since that time the existence of a defined HVS has been increasingly questioned. After the late 1980’s scientists began to increasingly voice doubts about the specific role of CO2 in the symptoms of HVS and the gold standard diagnostic test for HVS, the Hyperventilation Provocation Test (HVPT) (Garssen 1992; Hornsveld and Garssen 1996). While some researchers tried to develop new models that did not entirely dismiss hypocapnia in the pathophysiology of HVS (Hornsveld and Garssen 1996; Howell 1997; Folgering 1999; Wilhelm, Gertivz et al. 2001) others argued that HVS probably did not exist (Hornsveld 1997). In subsequent years, HVS became a controversial diagnosis; researchers tended to avoid it and clinicians struggled to find new names to describe patients with the combination of breathing abnormalities and unexplained symptoms (Hornsveld 1997). In recent years, researchers have begun to reconsider the importance of hyperventilation (Warburton and Jack 2006), and in the field of respiratory psychophysiology there has been a renewal of research interest in the role of hypocapnia in symptom production. This recent work tends to support a moderating role for CO2 in asthma and panic disorder (Howell 1990; Meuret and Ritz 2010).Since the beginning of the nineteenth century it has been known that central and peripheral neurovascular symptoms such as numbness, dizziness, muscle hypertonicity and tingling sensations could be brought on by voluntary forced ventilation (Bass 1989) which produces hypocapnia and respiratory alkalosis (Haldane 1908). The idea of a hyperventilation syndrome, which included these classic symptoms of hypocapnia and additional symptoms such as chest pain, palpitations, breathlessness, disorientation and anxiety, began after Kerr reported his use of the hyperventilation challenge to elicit these complaints in 35 patients whose symptoms were otherwise unexplained (Kerr 1937) (Chaitow 2002). The symptoms of one of the main diagnostic labels which preceded HVS, the “effort syndrome”, were subsequently attributed to hypocapnia and respiratory alkalosis (Soley and Shock 1938). The range of symptoms attributed to HVS eventually came to encompass a large number of symptoms of central and peripheral neurovascular, muscular, respiratory, cardiac, gastrointestinal origin (Soley 1938; Lewis 1953; Magarian 1982). Typical symptoms of HVS are shown in Table 1.
The definition of Hyperventilation Syndrome (HVS) has changed in the last 20 years as a result of controversy about the relationship of hypocapnia with the large number of symptoms that had over time come to be associated with this syndrome. The definition agreed upon by attendees of the 4th International Symposium on Psychophysiology in Southampton in 1984 is as follows:“Hyperventilation syndrome is a syndrome characterized by a variety of somatic symptoms induced by a physiologically inappropriate hyperventilation and usually produced in whole or in part by voluntary hyperventilation” p287, (Howell 1990). The definition of the HVS, the role of hypocapnia in producing symptoms historically associated with the HVS and the very existence of the HVS itself came to be questioned over the next decade (Gardner 1995). By 1997, it became clear that the definition proposed in Southampton in 1984 was insufficient. A new definition was proposed at the 3rd International Conference of Respiratory Psychophysiology in Nijmegen, The Netherlands. This definition continues to link medically unexplained physical symptoms with dysregulated breathing but decreases the emphasis on the importance of hypocapnia as an etiological factor:Hyperventilation Syndrome is “ a dysregulation of ventilation, causing hypocapnia, in the absence of somatic causes for hyperventilation, with symptoms not necessarily linked to hypocapnia” p73 (Molema and Folgering 1997).Despite this more flexible definition, HVS remains a controversial diagnosis. The following brief review of the history of the Hyperventilation Syndrome is presented to provide a context to understanding the controversies surrounding the Hyperventilation Syndrome.
It appears that the health issues faced by our children have to do with the social, environmental and dietary changes that have occurred over the last 50 -60 years.