Healthcare providers who do not routinely observe their patients'
breathing may miss helpful diagnostic information. Breathing assessment
can provide useful information regarding a client's emotional state and respiratory mechanics. Frequent sighs could signal depression. Low exhaled CO2 could indicate overbreathing, which can cause diverse symptoms.
While medical disorders fall outside most practitioners' scope of practice, they can share breathing assessment findings relevant to medical disorders with their client's physician. For example, a physician managing a client's hypertension might appreciate information about their apnea since it can contribute to this problem.
Our body uses 85-88% of blood CO2 to ensure a healthy acid-base balance to prevent our blood from becoming too acidic (acidosis) or basic (alkalosis). Artist: Dani S@unclebelang. This WEBTOON is part of our Real Genius series.
Inspiratory muscle activity (e.g., diaphragm and the external intercostal) increases metabolism. Muscles break down glucose and fatty acids to power contraction, which produces CO2 (Milic-Emili & Tyler, 1963; Swensen, 2017).
Slow-paced breathing with low tidal volumes retains more CO2 in arterial blood than when overbreathing. Tidal volume (TV) is the amount of air inhaled or exhaled during a normal breath (Fox & Rompolski, 2022).
Breathing plays a pivotal role in regulating the pH level of the blood. By adjusting the rate and depth of breathing, the body can control the amount of CO2 expelled, directly influencing the blood's acidity. This
regulation is vital for the proper functioning of enzymes and metabolic processes (Guyenet & Bayliss, 2015).
The table below shows how CO2 regulates blood pH and is redrawn from Gilbert (2005).
Breathing supports the efficient exchange of gases in the lungs, where oxygen is absorbed into the bloodstream, and CO2 is released for exhalation. This exchange is crucial for metabolic activities and energy production within cells (Hsia, 2023).
Slow-paced breathing releases more nitric oxide as blood CO2 rises and pH falls, resulting in vasodilation. Graphic is courtesy of Dr. Christopher Gilbert (2005).
The respiratory system also delivers odorants to the olfactory epithelium,
produces the airway pressure required for speech, anticipates cognitive and skeletal muscle metabolic demands, and
helps to modulate systems regulated by the autonomic nervous system (ANS), especially the cardiovascular system. Respiration is an important regulator of heart rate variability, consisting of beat-to-beat changes in the heart rhythm (Lorig, 2007). Check out the YouTube video The Respiratory System.
The Respiratory Cycle
We breathe about 20,000 times a day. Typical adult resting breathing rates are 12-14 breaths per minute (bpm; Khazan, 2019a). Disorders that affect respiration may raise rates to 18-28 bpm (Fried, 1987; Fried & Grimaldi, 1993).
The lungs cannot inflate themselves since they lack skeletal muscles. Instead, they are passively inflated by creating a partial vacuum by the diaphragm and external intercostal muscles (Gevirtz, Schwartz, & Lehrer, 2016).
During inhalation, contraction by the diaphragm and
external intercostal muscles ventilate the lungs.
The dome-shaped diaphragm muscle plays the lead role during inhalation. The
diaphragm comprises the floor of the thoracic cavity. When the diaphragm contracts, it flattens, and its dome drops, increasing the thoracic cavity volume. Contraction of the diaphragm pushes
the rectus abdominis muscle of the stomach down and out.
In relaxed breathing, a 1-cm descent creates a 1-3 mmHg pressure difference and moves 500 milliliters of air. In labored
breathing, a 10-cm descent produces a 100-mmHg pressure difference and transports 2-3 liters of air. The diaphragm
accounts for about 75% of air movement into the lungs during relaxed breathing.
The external intercostals
play a supporting role during inhalation. External intercostal muscle contraction pulls the ribs upward and
enlarges the thoracic cavity. The external intercostals account for about 25% of air movement into the lungs
during relaxed breathing.
The contraction of the diaphragm and the external intercostals expands the thoracic cavity, increases lung
volume, and decreases the pressure within the lungs below atmospheric pressure. This pressure difference causes air
to inflate the lungs until the alveolar pressure returns to atmospheric pressure.
The dome-shaped diaphragm muscle ascends during normal expiration.
Exhalation during relaxed breathing is produced by the relaxation of the diaphragm
and external intercostal muscles, contraction of the internal intercostals, the elastic recoil of the chest
wall and lungs, and surface tension. When the diaphragm relaxes, its dome moves upward. When the external intercostals relax, the
ribs move downward. These changes reduce the thoracic cavity volume and the lungs and increase the pressure within the lungs above atmospheric pressure. This pressure difference causes air to deflate the lungs until the
alveolar pressure returns to atmospheric pressure.
The BioGraph ® Infiniti display below shows healthy inhalation and
exhalation in which the abdomen gradually expands and contracts.
Types of Respiration
The term respiration refers to external, internal, and cellular processes.
External respiration transports gases in and out of our lungs. Internal respiration transports oxygen from the air we inhale, delivers it to our cells, and returns metabolic CO2 to the lungs for 12-15% to be exhaled and 85-88% retained to regulate pH (Khazan, 2021).
The alveoli collapse like “wet balloons” during normal breathing. Since deflated alveoli cannot absorb normal oxygen levels, the brain triggers sighs to reopen these air sacs. Humans initiate sighs every 5 minutes to increase oxygen delivery and activate the brain through double inhalation (Long, 2016).
The respiratory cycle consists of an
inspiratory phase, inspiratory pause, expiratory phase, and expiratory
pause. Abdominal respirometer excursion indexes respiratory amplitude (the peak-to-trough difference) and is often greatest during the inspiratory pause. The diagram below was adapted from Stern, Ray, and Quigley (1991).
Clinicians should examine all components of the respiratory
cycle—not just respiration rate—to understand their clients'
respiratory mechanics. Everyday activities like speaking and writing
checks may affect individual components differently.
Apnea, breath suspension, lowers
respiration rate. Clinicians teaching effortless breathing
training may instruct their clients to lengthen the expiratory pause with
respect to the inspiratory pause. The simple inspection of their respiration
rates will not show whether they have successfully changed the relative
durations of these two pauses. Finally, in heart rate variability (HRV)
biofeedback, clinicians encourage slow (5-7 bpm) and
rhythmic breathing.
Neural Control of Respiration
Respiration is controlled by a respiratory center in the medulla and pontine respiratory group. The dorsal respiratory group (DRG) and ventral respiratory group (VRG) are neuron clusters in two regions of the medulla. Pacemaker cells in the VRG (analogous to the heart's sinoatrial node) organize the basic breathing rhythm. Check out the Khan Academy YouTube video The Respiratory Center.
Medulla: DRG and VRG
The DRG's Role in Breathing
The DRG collects information from peripheral stretch and
chemoreceptors and distributes it to the VRG to modify its breathing rhythms. The DRG is responsible for normal quiet breathing. The majority of VRG neurons are inactive at this time. During forceful breathing, DRG neurons activate the VRG, stimulating the
diaphragm, sternocleidomastoid, pectoralis minor, scalene, and trapezius
muscles to contract
(Tortora & Derrickson, 2021).
The VRG's Role in Breathing
The phrenic and intercostal nerves transmit VRG inspiratory neuron action potentials to the diaphragm and external intercostal muscles. The contraction of these muscles expands the thoracic cavity and inflates the lungs.
VRG pacemaker cells influence the rate of DRG action potentials. VRG expiratory neurons inhibit DRG inspiratory neuron firing. Exhalation passively results from
diaphragm and external intercostal muscle relaxation and recoil by the chest wall and lungs. The DRG and VRG neurons' continuous reciprocal activity results in a 12-15 bpm respiratory rate, with 2-second inspiratory and 3-second expiratory phases.
Why Drug Overdoses Can be Lethal
An overdose of a CNS depressant like alcohol or morphine can completely inhibit VRG neurons in the medulla and stop breathing. The graphic below depicting the medulla is courtesy of Wikimedia Commons.
Cortical control of respiratory centers in the medulla and pons allows us to voluntarily stop or change our breathing patterns. This voluntary control protects against lung damage from water or toxic gases.
Inhaling through the mouth results in greater dead space and airway resistance compared to nose breathing (Tanaka, Morikawa, & Honda, 1988).
Mouth breathing is fine when there’s a need for large amounts of air, such as exercising, or when the nose is stuffed.
The nose acts as a natural filter, trapping dust, allergens, and other particulate matter before they can enter the lungs (Bjermer, 1999). Nasal passages also humidify and warm the air, protecting the respiratory tract from irritation and infection (Naclerio et al., 2007). Mouth breathing bypasses these natural defenses (Martel et al., 2020).
Inhaling through the nose releases nitric oxide, a gas that enhances the body’s ability to transport oxygen by dilating blood vessels, to the lungs. This process improves oxygen uptake in the blood, contributing to better overall cardiovascular health. Mouth breathing does not offer this benefit (Kimberly et al., 1996; Watso et al., 2023).
Chronic mouth breathing can lead to dry mouth, increasing the risk of dental decay and gum disease because saliva, which protects against bacteria and aids digestion, is reduced (Tamkin, 2020). Furthermore, the altered posture of the tongue and jaw can contribute to malformations in children, such as dental malocclusions and facial deformities (Lin et al., 2022).
Inhaling through the nose helps regulate the volume of inhaled air and maintains adequate levels of CO2 in the blood, which is necessary to efficiently release oxygen from hemoglobin to the body’s tissues (Prisca et al., 2024). Mouth breathing can lead to overbreathing and a reduction in CO2 levels, impairing oxygen delivery (LaComb et al., 2017; Tanaka, Morikawa, & Honda, 1988).
Exhaling through the nose cannot be regulated in the way that pursed-lips breathing can. Exhaling through pursed lips reduces inappropriate breathing volume when the cause is emotion rather than exercise demand.
Many people favor practicing breathing by inhaling through the nose and exhaling through the mouth, so that's a compromise between the two that makes sense.
Nasal inhalation may accelerate our response to physical threats and impact fear and memory. During panic attacks, breathing is faster, and we spend more time inhaling (Zelano et al., 2016). Check out the YouTube video How you breathe affects memory and fear.
Clinicians encounter six abnormal breathing patterns which reduce oxygen
delivery to the lungs: thoracic breathing, clavicular breathing, reverse
breathing, overbreathing, hyperventilation, and apnea.
Thoracic Breathing
In thoracic breathing, the chest muscles are mainly responsible for breathing. The external intercostals lift the rib cage up and out.
The diaphragm is pushed upward as the abdomen is drawn in. Upward and outward movement of the ribs enlarges the thoracic cavity
producing a partial vacuum. Negative pressure expands the lungs but is
too weak to ventilate their lower lobes. Thoracic breathing reduces ventilation since
the lower lobes receive a disproportionate share of the blood supply due
to gravity.
Thoracic breathing expends excessive energy,
incompletely ventilates the lungs, and strains our accessory muscles.
In the BioGraph ® Infiniti screen below, the abdominal (blue trace) strain gauge exhibits minimal excursion,
and the
respiration rate exceeds the desired 5-7 breaths-per-minute range.
Are you a thoracic breather? Place your left hand on your chest and your
right hand on your navel. If both hands shallowly rise and fall at about
the same time, you are breathing thoracically.
Clavicular Breathing
In clavicular breathing, the chest rises, and the collarbones are elevated
to draw the abdomen in and raise the diaphragm (Khazan, 2021). Clavicular breathing may
accompany thoracic breathing. Patients may breathe through their mouths to
increase air intake. This pattern provides minimal pulmonary ventilation.
Over time, the accessory muscles (sternocleidomastoid, pectoralis minor,
scalene, and trapezius) use more oxygen than clavicular breathing provides.
Clavicular breathing may be accompanied by thoracic and mouth breathing, produce an oxygen deficit, reduce CO2, and cause overbreathing.
In the BioGraph ® Infiniti screen below, the purple trace represents the
chest strain gauge, and the red trace represents accessory SEMG activity.
Note the rapid shallow chest movement and fluctuating accessory
SEMG values that increase with the shoulder elevation accompanying
each inhalation.
Are you a clavicular breather? Have an observer lightly place one hand on
your shoulder (the observer's shoulder must be relaxed). If this hand
rises as you inhale, then you show clavicular breathing.
Reverse Breathing
Reverse breathing, where the abdomen expands during exhalation and
contracts during inhalation, often accompanies thoracic breathing and results in incomplete ventilation of the
lungs.
In the BioGraph ® Infiniti screen below, the client starts at the left
with inhalation, followed by exhalation. Note how the stomach contracts
during inhalation (falling blue trace) and expands during exhalation (rising
blue trace). This pattern is the opposite of healthy breathing.
Are you a
reverse breather? If the hand on your stomach falls and the hand on your
chest rises when you inhale, you are reverse breathing.
Reverse breathing
expends excessive energy and incompletely ventilates the lungs.
Overbreathing
Overbreathing
is a mismatch between breathing rate and depth (Khazan, 2021). This disparity may involve rapid breathing, increased tidal volume (the amount of air exhaled during a breath), and more subtle behaviors like gasps and sighs.
Gasps and sighs involve the quick intake of a large air volume, accompanied by breath-holding. They may comprise part of a defensive reaction. When clients expel excessive CO2, this lowers end-tidal CO2 (the percentage of CO2 at the end of exhalation) and causes hypocapnia, which is deficient CO2.
Acute overbreathing produces various symptoms.
Hypocapnia Disrupts Homeostasis
Hypocapnia disrupts homeostasis by disturbing the body's acid-base (pH) and electrolyte balance, blood flow, and oxygen delivery. Hypocapnia may force the kidneys to expel bicarbonates to restore pH balance (Khazan, 2021).
Electrolytes are substances like acids or salts that can dissociate into free ions when dissolved (e.g., NaCl → Na+ + Cl-). Hypocapnia deprives cells (e.g., neurons, cardiac muscle, and skeletal muscle) of the ions (Ca+2 and Na+) required for typical membrane potentials and communication with other cells.
The Effects of Ca+2 Movement
Hypocapnia can move Ca+2 from the interstitial fluid into muscle cells with disastrous results. In skeletal muscle, calcium entry can cause spasms, fatigue, and weakness. In blood vessel smooth muscle, it can produce vasoconstriction. In the bronchioles of the lungs, it can trigger bronchoconstriction. Finally, in GI tract smooth muscle, it can result in nausea and change in motility.
Healthy end-tidal CO2 values range from 35-45 mmHg. Moderate overbreathing can reduce oxygen delivery to the brain by 30%-40%, and
severe overbreathing can reduce it by 60%.
Overbreathing can produce acute and chronic vasoconstriction effects and reduced delivery of oxygen and glucose to body tissues, especially the brain (Khazan, 2013).
The SPECT scan created by Dr. Scott Woods below shows the effect of overbreathing on brain metabolism. Darker colors represent reduced metabolism and compromised cortical functioning.
The Effects of Chronic Overbreathing
Clients who overbreathe may experience chronic hypocapnia.
Since the body cannot function with sustained high pH, the kidneys excrete bicarbonates to return pH to near-normal levels. Bicarbonates are salts of carbonic acid that contain HC03. Acid buffering can only restore homeostasis in the short run because increased metabolism raises acidity until needed bicarbonates are depleted. When this happens, clients experience fatigue, muscle pain, reduced physical endurance, and a sodium deficit. Acidosis may increase overbreathing in a failed attempt to reduce acidity (Khazan, 2021).
Why Do Clients Overbreathe?
Clients overbreathe as part of the fight-or-flight response in response to stressors, when they experience difficult emotions, and when they suffer chronic pain. They can learn this dysfunctional breathing pattern through classical and operant conditioning and social learning.
If clients practice overbreathing long enough, it can become a habit when this lowers the body's setpoint for CO2. When breathing slows, the respiratory centers attempt to restore low CO2 levels by removing it through behaviors like breath-holding, sighing, and yawning (Gevirtz, Schwartz, & Lehrer, 2016). Reduced blood CO2 levels may contribute to asthma, panic, phobia, and pain disorders like chronic low
back pain.
Overbreathing and Hyperventilation Have Different Clinical Presentations
Clients who present with HVS breathe thoracically, deeply, and rapidly (over 20 bpm) using accessory muscles (the sternum moves forward and upward) and restricting diaphragm movement. Rapid breathing can lower end-tidal CO2 from 5% to 2.5%, although many patients have normal values during attacks (Kern, 2021).
Like overbreathing, this pattern exceeds the body's need to eliminate CO2, reduces oxygen delivery
to body tissues and NO release, and curtails their supply of glucose (Khazan, 2013). Check out the YouTube video Breathing Pattern Disorders Such as Hyperventilation.
The BioGraph ® Infiniti display below shows the shallow, rapid breathing
that characterizes hyperventilation.
In contrast to HVS, overbreathing is usually so
subtle that the patients are unaware that their sighs and yawns produce hypocapnia.
Apnea
Apnea involves the suspension of breathing. While commonly associated with sleep, breath-holding while awake may occur during stressful situations as part of a defensive response. A client may also hold their breath during ordinary activities like opening a jar,
speaking, or writing a check. Episodes of apnea decrease ventilation and
may increase blood pressure.
In the BioGraph ® Infiniti display below, the blue abdominal strain gauge trace briefly flattens when the patient suspends breathing after the second breath.
Glossary
accessory muscles: the sternocleidomastoid, pectoralis minor, scalene, and
trapezius muscles, which are used during forceful breathing, as well as during clavicular and thoracic
breathing.
acidosis: a decrease in the normal alkalinity of the blood or tissues, leading to a lower pH level. It can be caused by an increase in acid production, a decrease in acid excretion, or a loss of bicarbonate, which is a base that helps neutralize acids in the body.
apnea: breath suspension.
bicarbonates: salts of carbonic acid that contain HC03.
Bohr effect: the influence of carbon dioxide on hemoglobin release of nitric oxide and oxygen.
carbon dioxide: a gas produced by cellular metabolism, crucial for regulating breathing, maintaining blood pH balance, and facilitating oxygen delivery to tissues.
cerebral cortex: the 2-4 millimeter-thick outer layers covering the cerebral hemispheres containing circuitry essential to complex brain functions like cognition and consciousness.
clavicular breathing: a breathing pattern that primarily relies on the
external intercostals and the accessory muscles to inflate the lungs, resulting in a more rapid respiration
rate, excessive energy consumption, and incomplete ventilation of the lungs.
diaphragm: the dome-shaped muscle whose contraction enlarges the vertical
diameter of the chest cavity and accounts for about 75% of air movement into the lungs during relaxed
breathing.
dorsal respiratory group (DRG): neuron clusters in the brainstem's medulla that collect information from peripheral stretch and chemoreceptors and distribute this information to the VRG to modify its breathing rhythms.
end-tidal CO2: the percentage of CO2 in exhaled air at the end of exhalation.
external intercostals: the muscles of inhalation that pull the ribs upward and
enlarge the thoracic cavity. The external intercostals account for about 25% of air movement into the lungs
during relaxed breathing.
heart rate variability (HRV): beat-to-beat changes in heart rate, including changes in the R-R intervals between consecutive heartbeats.
hemoglobin: a red blood cell protein that carries oxygen throughout the circulatory system.
hypercapnia: a condition characterized by an abnormally high level of carbon dioxide (CO2) in the blood.
hyperventilation (HV): a syndrome in which deep and rapid breathing cause breathlessness and reduce end-tidal
CO2 below 5%, exceeding the body's need to eliminate CO2.
hypocapnia: decreased CO2 in arterial blood.
inspiratory muscles: the diaphragm and external intercostals.
metabolic acidosis: a disturbance characterized by a decrease in the body's bicarbonate levels or an increase in the production of acids, leading to a reduction in the arterial blood pH below 7.35. This condition can result from increased acid production (such as ketoacidosis or lactic acidosis), reduced kidney acid secretion, or significant bicarbonate losses.
nitric oxide (NO): a gaseous neurotransmitter that promotes vasodilation and long-term potentiation.
overbreathing: a mismatch between breathing rate and depth due to excessive breathing effort and subtle breathing behaviors like sighs and yawns can reduce arterial CO2.
oxygen saturation: a measure of the percentage of hemoglobin binding sites in the bloodstream occupied by oxygen.
pH: the power of hydrogen; the acidity or basicity of an aqueous solution determined by the concentration of hydrogen ions.
pons: a brainstem structure above the medulla containing breathing
centers that adjust VRG breathing rhythms based on descending input from brain structures and peripheral
sensory input.
pontine respiratory group (PRG): neurons located in the pons that communicate with the dorsal respiratory group (DRG) in the medulla to modify the basic breathing rhythm.
rectus abdominis: a muscle of forceful expiration that depresses the
inferior ribs and compresses the abdominal viscera to push the diaphragm upward.
respiratory acidosis: a state in which decreased ventilation (hypoventilation) leads to an increase in carbon dioxide concentration and a decrease in blood pH. This condition is often due to impaired lung function, chest injuries, or diseases that affect the respiratory muscles or control of breathing.
respiratory alkalosis: a condition characterized by elevated blood pH due to excessive carbon dioxide exhalation, typically caused by hyperventilation.
respiratory amplitude: the excursion of an abdominal strain gauge.
respiratory cycle: an inspiratory phase, inspiratory pause,
expiratory phase, and expiratory pause.
respiratory membrane: the site of respiratory gas exchange that is comprised
by alveolar and capillary walls.
reverse breathing: a dysfunctional breathing pattern in which the abdomen expands during exhalation and contracts
during inhalation, often resulting in incomplete ventilation of the lungs.
thoracic breathing: a dysfunctional breathing pattern that relies primarily on the
external intercostals to inflate the lungs, resulting in a more rapid respiration rate, excessive energy
consumption, and insufficient lung ventilation.
tidal volume: the amount of air inhaled or exhaled during a normal breath.
ventral respiratory group (VRG): neurons located in the medulla that initiate inhalation and exhalation.
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Assignment
Now that you have completed this unit, think about your own breathing
pattern and the patterns you most often see in your clients.
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