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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