Download Ashley Craig - Breath rate control and managing chronic pain

Breath rate control and managing chronic pain
Dr Ashley Craig
Professor of Rehabilitation Studies
Kolling Institute of Medical Research
Sydney Medical School-Northern, The University of Sydney, NSW Australia
1
Senior Clinical Psychologist
READ Clinic, Erina NSW
Objectives
1) To describe the process involved when someone is
anxious
2) To discuss the role of parasympathetic activity,
concentrating on the role of the vagus nerve
3) To discuss the actions of the respiratory system
4) To discuss slow breathing and vagal nerve control
5) Applying slow breathing to control chronic pain
Most of us know this feeling!!
Or perhaps this feeling!!
Anxiety
Anxiety is an emotional state associated with:
(1) Cognitive component of increased attentional focus on
threat to the integrity of the individual
(1) a complex sympathetic arousal response
(1) behaviour aimed at avoiding threatening situations for the
individual
Emotions are subjective conscious experiences
that influence our entire being
How does stress effect us? Two processes:
1. Allostasis: the process of maintaining stability (homeostasis) through the release
of stress hormones, peripheral nervous system mediators and coping strategies
2. Allostatic load: the wear and tear on the body and brain caused by allostasis,
especially when mediators are dysregulated, eg. not turned off when stress is over or
not turned on adequately when they are needed (eg. when a person is depressed)
Important brain structures involved in emotional and
stress regulation
1. The ascending reticular activating system (RAS) is an area of the
brain responsible for regulating arousal and sleep-wake transitions
2. The RAS has neuronal circuits connecting to the cortex via the
limbic and hypothalamus
3. The descending RAS connects to cerebellum and to PNS nerves
1. The limbic system includes the hippocampus, amygdala, thalamic
nuclei, septum, cingulate gyrus, and fornix, and is involved in
emotional regulation, behaviour and memory
2. The limbic system strongly influences the endocrine and
autonomic nervous system
3. The hypothalamus also links the nervous system to the endocrine
system via the pituitary gland (hypophysis)
Emotion and stress regulation circuits
Two main circuits exist:
1. The hypothalamic-pituitary-adrenal (HPA) axis.
Long-term stress response
2. The sympathetic-adreno-medullary system (SAM).
Short-term stress response
Through these two systems, the brain influences all body
organs during stressful/ emotional times
Hypothalamic-pituitary-adrenal axis
In this response, the hypothalamus secretes a hormone called CRH
(corticotrophin releasing hormone).
CRH stimulates the pituitary gland (also located in the brain) to produce
ACTH (adreno-corticotropic hormone).
ACTH stimulates the adrenal cortex
(outer part of the adrenal glands) to release
stress hormones like glucocorticoids (eg.
cortisol) and mineralcorticoids (aldosterone
which influences water retention)
Chronic activation of the hypothalamic-pituitaryadrenal axis
Research has shown that chronic activation of the HPA fight/flight
response can be a factor in causing a number of psychological and
physiological health problems.
Monoamine neurotransmitters that regulate the HPA axis include
dopamine (adrenaline), serotonin (5 Hydroxytryptamine or 5HT,
serotonergic neurons in CNS) and norepinephrine (noradrenaline)
Some antidepressants attempt to regulate the HPA Axis function in order
to improve mood and anxiety, and which also have a beneficial
independent impact on chronic pain:
SNRIs (Pristiq, Effexor, Cymbalta),
Tricyclics (TCAs: Amitriptyline: Endep)
Tetracyclics (eg. Mirtazapine or Avanza)
Hypothalamic-pituitary-adrenal
axis hormones
Negative feedback loops and stress
Oxytocin (cuddle hormone) release
Example: positive social interaction and touch, acts to suppress the HPA axis
and counteracts stress, promoting positive mental and physical health effects
Cortisol produced in the adrenal cortex will negatively feedback to inhibit
both the hypothalamus and the pituitary gland. This reduces the secretion of
CRH, and therefore turns off the HPA response
Opioid secretion and stress, and feedback loops
Activation of the HPA axis stimulates release of opioids
This reciprocally inhibits activity of the stress system
This produces analgesia through projections to the hindbrain (pons,
cerebellum, medulla) and spinal cord
The sympathetic-adrenomedullary system (SAM)
Electrical impulses from the hypothalamus travel along sympathetic nerves
that directly connect to the adrenal glands (on top of the kidneys) and
stimulate the release of stress hormones adrenaline and noradrenaline
(catecholamines)
The body cannot sustain this response for long as it would become
exhausted. If the stressor is more chronic, then the longer-term HPA
fight/flight response is triggered
Autonomic nervous system
Parasympathetic nervous system
The parasympathetic nervous system (PNS) is responsible for stimulation of
"rest-and-digest" activities that occur when the body is at rest, including sexual
arousal, salivation, urination, digestion, and defecation
The PNS influences heart rate (HR) by the vagus nerve (10th cranial nerve)
If we manipulate breath rate, we will also effect HR, BP and anxiety
For example, if we begin to breathe slowly, HR, BP and anxiety all drop, and
mood improves. The opposite is true.
Autonomic nervous system
Cranial nerves: peripheral nervous system
CN I – Olfactory
CN II – Optic
CN III – Oculomotor
CN IV – Trochlear
CN V – Trigeminal
CN VI – Abducens
CN VII – Facial
CN VIII – Vestibulocochlear
CN IX – Glossopharyngeal
CN X – Vagus
CN XI – Accessory
CN XII – Hypoglossal
The respiratory system
When breathing in (inspiration), air passes
through the trachea, into the bronchi, then the
bronchioles, then into the respiratory
bronchioles (called an upside down tree),
which contain the pulmonary alveoli, the
terminal ends of the respiratory tree
The alveolar membrane is the gas-exchange
surface. CO2 rich blood is pumped from the
body into the alveolar blood vessels where,
through diffusion, it releases its CO2 and
absorbs O2
lungs
It takes some effort to breathe in as the alveoli
need to be inflated
while breathing out is easier due to elastic
recoil.
The respiratory system's major functions are to provide an adequate O2
supply to meet energy production requirements and maintain a suitable
acid-base status by removing CO2 from the body.
Control of the respiratory system is through a central respiratory
pacemaker located within the medulla of the brainstem.
Neural output travels from this center through the spinal cord to the
muscles of respiration.
The changes are made through muscles such as the diaphragm and
intercostal muscles, which contract and relax to produce a rhythmic
respiratory rate and pattern.
The central respiratory pacemaker in the medulla is influenced by
several factors, resulting in change in breath rate. These include:
Chemical:
the pacemaker responds to changes in pH (due to changes in
concentration of CO2 and O2 in the blood) leading to changes in breath
rate. Too much CO2 and pH drops while too little CO2 and pH rises (say
due to hyperventilation)
Mechanical:
elasticity of lungs: the respiratory system chooses a breath rate that
requires least amount of mechanical work while maintaining adequate
gas exchange
Neural or top down:
sleep normally lowers breath rate (except perhaps in dreams), and
anxiety increases breath rate, perhaps leading to hyperventilation
Hyperventilation
Fast breathing say over 20 breaths per minute (BPM) leads to
dysfunction, such as build up of toxins in the blood, a fall in CO2, and if
prolonged, a condition called hypocapnia, that is, a rise in blood pH.
This rise in blood pH is known as respiratory alkalosis, that is, when the
respiratory system removes more carbon dioxide than is produced in the
tissues (such as during stress and anxiety/ panic).
When hyperventilation leads to respiratory alkalosis, blood vessels
constrict, causing a number of physical symptoms: dizziness, tingling in
the lips, hands or feet, headache, weakness, fainting, seizures and noncardiac chest pain (though chest pain can be caused by things such as
gastrointestinal problems and chest muscle strains).
Respiratory rate (BPM) can then be increased by the pacemaker in
attempts to lower this condition, perhaps worsening the situation?
Breathing and anxiety
Breathing is an integral component of interoceptive processing, that is, how
we perceive feelings from our bodies that determine our mood, sense of
well‐being and emotions
Changes in breathing can be both the consequence of an increased level of
anxiety or other conditions like physical activity
Therefore assessing breathing is a useful physiological marker of anxiety
and possibly pain
Paulus (2010). Depression and Anxiety. doi: 10.1002/da.22076
Zautra et al., (2010). Pain, 149, 12–18. doi:10.1016/j.pain.2009.10.001
What is your breath rate?
The Bohr Effect
The amount of CO2 in your blood is directly related to how
quickly you breathe. The quicker you breathe the more CO2
you lose when you exhale.
This usually does not apply to oxygen, as your blood is near saturated
with O2 and you would have to reduce your breathing substantially before
O2 was affected.
An increase in blood CO2 concentration leading to a decrease in blood pH,
will result in haemoglobin cells releasing their load of oxygen.
Conversely, a decrease in CO2 provokes an increase in pH, which results
in haemoglobin picking up more oxygen
If you hyperventilate, your CO2 will be too low, while your O2 will OK.
This is part of the problem that causes the unwell symptoms associated
with hyperventilation and is called the Bohr Effect.
Breathing and chronic pain
Anxiety disorders such as Panic Disorder and trauma disorders like PTSD are
associated with altered breathing characteristics or altered responses to
manipulating breathing (Bryant et al., (2008). Journal Clinical Psychiatry, 69, 1694-1701;
Paulus (2010))
For example, a BPM of over 20 has a definite risk of psychological disorder like
PTSD (Bryant et al., 2008)
Pain can be regarded as a negative emotion that is part of the arousal/ stress
system characterized by increased sympathetic activation
People with some forms of chronic pain may have deficits in their
parasympathetic branch of the ANS, needed for down-regulation of negative
emotion and pain experiences
In a study investigating the benefits of slow breathing on chronic pain, lower
breathing rates were found to be a clinically useful target in interventions for
patients in pain.
Slow breathing exercises reduced ratings of pain intensity and unpleasantness,
as well as negative mood states
The authors concluded that reductions in pain and negative affect may be
expected when people are taught to halve their respiration rate
Zautra et al., (2010). The effects of slow breathing on affective responses to pain
stimuli: An experimental study. Pain, 149, 12–18.
doi:10.1016/j.pain.2009.10.001
Parasympathetic nervous system
Resting HR fluctuates with the breathing cycle. Breathe in and HR
increases. Breathe out and HR decreases. This is called respiratory sinus
arrhythmia (RSA)
RSA is a measure of vagal activity (tone), that is the vagal control of the
heart
Large variation in RSA: good vagal tone; small RSA: poor vagal tone.
During sympathetic nervous system (SNS) activity, vagal control withdraws,
allowing increased HR and BP
Parasympathetic nervous system:
vagal tone control
Evidence suggests that anxious people have low RSA (poor vagal tone)
and are vulnerable to depression
This may be true of people with chronic pain? Greater levels of RSA (or
greater parasympathetic activity) was found to be a promising indicator
of physiological resilience to pain (Sturgeon et al., 2014 Respiratory sinus
arrhythmia: a marker of resilience to pain induction. doi:10.1007/s12529-014-9386-6)
Those with high RSA are less prone to hypertension, heart disease,
depression and chronic pain
A person can learn to enhance vagal tone (increase RSA) through slowed
breathing and extended breathing out exercises
Learning skills that establish a slow breath rate
First
Establish baseline BPM. This involves counting breaths in over say, a one
minute period. Only do this after sitting in a relaxed manner for 20
minutes or so.
When counting, do not alter the way you breathe when you count your
BPM.
This should be done over at least one month to determine trends.
Second
Learning to breath slowly: begin with a very slow breathing cycle, that is, a 10
second breathing cycle or 6 BPM
•
•
•
•
•
Take in a normal breath through your nose with your mouth closed;
Second, hold your breath while you count to five;
Breathe out or exhale very slowly with your mouth open or closed, whichever
feels most comfortable. Say 'calm' or 'relax' to yourself silently;
After breathing out, do not breathe in immediately. Wait two seconds before
breathing in;
Then repeat the process for a period of at least 5 minutes. If it feels odd,
persist. You will enjoy the feeling of calm that this exercise creates.
Practise this type of breathing at least twice a day, once in the morning and once in
the afternoon or in the evening. Regular slow breathing practice reduces baseline
BPM.
Use this slow breathing skill when you notice your BPM increasing.
Breathing apps
iPhone
The “Breathing Zone” app can be downloaded for iPhone, Ipod or iPad for
under $5. It provides guidance on slow breathing
Web address: https://itunes.apple.com/au/app/breathing-zone-relaxingbreathing/id369838631?mt=8
Android
app called “Paced Breathing” can be found at the following website:
https://play.google.com/store/apps/details?id=com.apps.paced.breathing&hl=
en
Breathing Zone can be found at:
https://play.google.com/store/apps/details?id=com.breathing.zone&hl=en
Thank you