Health-care providers who do not routinely observe their patients' breathing patterns may miss valuable diagnostic information. Patient respiratory patterns can disclose a chronic startle response and provide valuable information about a patient's current emotional state, respiratory disorders and undiagnosed medical conditions (e.g., kidney disease), risk for heart attack, and respiratory involvement in psychophysiological disorders like essential hypertension.



This unit discusses Descriptions of most commonly employed biofeedback modalities: Respiration (III-A 2) and Structure and function of the autonomic nervous system (V-A 3).

Students completing this unit will be able to discuss:

  1. Descriptions of most commonly employed biofeedback modalities: Respiration
    A. Characteristic signals
  2. Physiological mechanisms underlying commonly employed biofeedback modalities, including respiration



You breathe about 20,000 times a day. Males breathe 12-14 breaths per minute compared to 14-16 breaths per minute for females. Effortless breathing through the nose ranges from 3-6 breaths per minute. Hyperventilation often exceeds 20 breaths per minute (Fried, 1990).

The respiratory cycle consists of inspiration (breathing in) and expiration (breathing out), which are controlled by separate mechanisms. During healthy inspiration, the diaphragm and external intercostal muscles contract. Downward movement of the dome-shaped diaphragm and upward pull on the ribs by the external intercostals enlarge the thoracic cavity producing a partial vacuum. Negative pressure expands the lungs, ventilates the lower lobes of the lungs, and aids venous return to the heart (reducing the heart's workload). Contraction of the diaphragm pushes the rectus abdominis muscle (of the stomach) down and out.







 

 

 

 

                                 



During normal expiration, both the diaphragm and external intercostal muscles relax. The diaphragm moves upward (due to elasticity) and the ribs move downward decreasing the thoracic cavity. Also, contraction of the rectus abdominis compresses the abdominal viscera pushing the diaphragm upward. Increased pressure within the lungs produces elastic recoil of the chest wall and lungs, and contracts the lungs (Tortora & Derrickson, 2006).
















                             



The BioGraph « Infiniti display below shows healthy inspiration and expiration in which the abdomen gradually expands and then contracts.





Respiratory gases are exchanged (between the lungs and blood) across the alveolar-capillary membrane in the lungs. The lungs contain an estimated 30 million alveoli (air sacs) that create an incredible 753 ft2 surface for gas exchange (Tortora & Derrickson, 2006).



Caption: This image illustrates the respiratory division of the respiratory system. The respiratory tubes, or bronchioles, end in minute alveoli, each of which is surrounded by an extensive capillary network. The alveoli, alveolar sac, pulmonary venule and pulmonary arteriole, bronchiole, and the capillary network on surface of the alveolus are represented.



The respiratory cycle consists of an inspiratory phase, inspiratory pause, expiratory phase, and expiratory pause. The excursion of an abdominal strain gauge, which indexes amplitude, is often greatest during the inspiratory pause.


                            

Clinicians should examine all components of the respiratory cycleŚnot just respiration rateŚto understand their client's 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. 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 breaths per minute) and rhythmic breathing.




Respiration is controlled by the rhythmicity area in the medulla, the pneumotaxic area and apneustic area in the pons, and the cortex.

The rhythmicity area in the medulla contains separate inspiratory and expiratory regions. During normal respiration, the inspiratory area stimulates the respiratory muscles for 2 seconds. The diaphragm and external intercostals contract producing normal inspiration. The inspiratory area then shuts down for 3 seconds. The diaphragm and external intercostals relax producing expiration.




      


During high levels of respiration, the inspiratory area stimulates the diaphragm, sternocleidomastoid, pectoralis minor, scalene, and trapezius muscles to contract producing forced inspiration. Signals from the inspiratory area also activate the expiratory area which orders the internal intercostals, and abdominal muscles to contract producing forced expiration.

The pneumotaxic area in the upper pons and apneustic area in the lower pons coordinate the transition between inspiration and expiration. The pneumotaxic area constantly sends inhibitory impulses to the inspiratory area that limit inspiration (to prevent lung overfilling) and assist expiration. In contrast, the apneustic area sends excitatory impulses to the inspiratory area (only when the pneumotaxic area is inactive) which prolong inspiration and inhibit expiration.




      


The cerebral cortex's control of brainstem respiratory centers allows us to voluntarily stop or change our breathing pattern. This voluntary control protects against lung damage from water or toxic gases. The rise of CO2 and H+ in the blood limits our ability to stop breathing by stimulating the inspiratory area when a critical level is reached. This homeostatic mechanism prevents us from killing ourselves by holding our breath (Tortora & Derrickson, 2006).




       




Clinicians encounter five abnormal breathing patterns which reduce oxygen delivery to the lungs: thoracic breathing, clavicular breathing, reverse breathing, hyperventilation, and apnea.
 


In thoracic breathing, external intercostals lift the rib cage up and out. The diaphragm is pushed upward as the abdomen is drawn in. Abdominal contraction compresses the abdominal viscera pushing the diaphragm upward. 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. This reduces ventilation since the lower lobes receive a disproportionate share of the blood supply due to gravity. Thoracic breathing (with or without reverse breathing) expends excessive energy and incompletely ventilates the lungs.

In the BioGraph « Infiniti screen below, the abdominal (red trace) and thoracic strain gauges (blue trace) exhibit 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.



In clavicular breathing, the chest rises and the collarbones are elevated to draw the abdomen in and raise the diaphragm. Clavicular breathing may accompany thoracic breathing. Patients mouth breathe 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 (deficit spending).

In the BioGraph « Infiniti screen below, the blue trace represents the chest strain gauge and the red trace represents accessory SEMG activity. Note the rapid shallow rapid chest movement and fluctuating accessory SEMG values that increase with the shoulder elevation that accompanies each inspiration.





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 are showing clavicular breathing.



Reverse breathing, where the abdomen expands during expiration and contracts during inspiration, may accompany thoracic breathing.

In the BioGraph « Infiniti screen below, the client starts at the left with inspiration followed by expiration. Note how the stomach contracts during inspiration (falling trace) and expands during expiration (rising trace). This 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.

 


From 10-25% of the population hyperventilates. This disorder accounts for about 60% of major city ambulance calls. Phobia provides the best model of hyperventilation. Breathing is predominantly thoracic. These patients can breathe very rapidly (over 20 breaths per minute) using accessory muscles (the sternum moves forward and upward) and restricting diaphragm movement. Their rapid breathing lowers end-tidal CO2 from 5% to 2.5%, reducing oxygen perfusion of body tissues.

The BioGraph « Infiniti display below shows the shallow rapid breathing that characterizes hyperventilation.






A client suspends breathing during an episode of apnea. While awake, a patient may present with this symptom when engaged in 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 patient suspends breathing several times as shown by a relatively flat abdominal strain gauge trace.















Now that you have completed this module, think about your own breathing pattern and the patterns you most often see in your clients.




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Fox, S. I. (2006). Human physiology (9th ed.). New York: McGraw-Hill.

Fried, R. (1987). The hyperventilation syndrome: Research and clinical treatment. Baltimore: John Hopkins University Press.

Peper, E., Harvey, R., Lin, I., Tylova, H., & Moss, D. (in press). Is there more to blood volume pulse than heart rate variability, respiratory sinus arrhythmia, and cardio-respiratory synchrony? Biofeedback.

Peper, E., & Tibbetts, V. (1992). Fifteen-month follow-up with asthmatics utilizing EMG/incentive inspirometer feedback. Biofeedback and Self-regulation, 17(2), 143-151.

M. S. Schwartz, & F. Andrasik (Eds.). (2003). Biofeedback: A practitioner's guide (3rd ed.). New York: The Guilford Press.

Stern, R. M., Ray, W. J., & Quigley, K. S. (2001). Psychophysiological recording (2nd ed.). New York: Oxford University Press.

Tortora, G. J., & Derrickson, B. H. (2006). Principles of anatomy and physiology (11th ed.). New York: John Wiley & Sons, Inc.