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Basic respiratory physiology for the sleep technology.

Sometimes when we are so focused on getting our patient's CPAP titrated to just the right pressure before time runs out and they wake up, we miss seeing "the forest through the trees". We look so closely at the "airflow" channel to determine if there are any respiratory events that we miss seeing the patient's overall breathing patterns. We sometimes miss subtle changes in respiratory rate or forget to consider how we have changed the patient's minute ventilation and therefore caused a change in breathing patterns that does not need to be "fixed". Until full 12-24 month educational programs are available for sleep medicine technology, it is not likely many working technologists will have had the opportunity to be trained in more than the most basic operating principles of data acquisition equipment and CPAP titration.

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Even skilled respiratory therapists need a review of basic respiratory physiology with the addition of information about how onset of sleep affects that physiology. Additionally, they need to recognize the differences between general ventilator management and non-invasive CPAP titration during sleep as they relate to the patient's breathing patterns and effectiveness of their ventilation. Most people don't think of non-invasive CPAP (NCPAP) as ventilatory therapy. Let's think about that. If a patient's minute ventilation is low due to apneas and with NCPAP they are able to move an average, normal tidal volume of air with each breath, we have increased their minute ventilation and can expect physiological changes as result. Let's start with a few basic terms:

Tidal Volume: The volume of air that enters the lungs during inspiration and leaves the lungs during expiration during a normal breath, about 5-600cc for the normal adult.

Minute Ventilation: The amount of air moved in or out in one minute. The tidal volume times the respiratory rate.

Resting end-expiratory level: The point at which the tendency of the lungs to collapse inward and the rib cage to spring outward are in balance. It is easiest to take a normal breath in from this point.

Work of Breathing: The oxygen usage and carbon dioxide production cost of breathing. Normally 5% of total oxygen consumption.

Arterial blood pH: The acidity or alkalinity of arterial blood. Normally about 7.4. Determined primarily by the relationship between dissolved carbon dioxide and the bicarbonate ion concentration in the blood.

PaCO2: Partial pressure of carbon dioxide in arterial blood. Usually about 40 mmHg. Higher levels make the blood more acidic and therefore lower the pH.

HCO3: Bicarbonate ion. Higher concentrations in the blood make it more alkalotic and raise the pH.

Control of Breathing: Influenced by many factors but primarily by the pH of the blood.

We can change the amount of CO2 in our blood quickly and influence our drive to breathe. To demonstrate this you can breathe fast for about 15 seconds ending with a big inspiration and exhaling normally to where it stops coming out, your end expiratory point. Just sit there and wait until you have an urge to breathe. The feeling that you need to breathe is because the CO2 has built up in your blood to the point it triggers you to breathe. Now put an oximeter on your finger. Let your air out to your normal end expiratory point and don't breathe until you can't stand it any more. Did you oxygen saturation go down? Probably not. Your urge to breathe was the result of high concentrations of CO2 in your blood, not low oxygen. Some patients have lung disease or other respiratory pathology that chronically limits their ability to achieve a minute ventilation high enough to keep their PaCO2 in a normal range and their body compensates for the high PaCO2 and low pH by allowing the kidneys to retain more of the alkalotic bicarbonate ion (HCO3-) to neutralize the acidic CO2 and bring the pH back toward the normal 7.4. It takes the body hours to retain or eliminate HCO3 but only seconds to eliminate CO2 by breathing faster. Or it can quickly retain C02 by breathing slower to balance the pH if HC03 is elevated. If disease makes it difficult to eliminate CO2 adequately it gets used to the low, acidotic pH and starts using its back up method to stimulate breathing, the oxygen concentration in the blood, PaO2. When the oxygen saturation falls to a given point, a breath is stimulated ignoring the volatile PaCO2 as a stimulus to breathe.

When we start CPAP and especially when we initiate BiLevel therapy, we increase minute ventilation and therefore decrease CO2, raise the pH, and signal the body to breath less. It does this by not breathing at all momentarily (like our experiment), breathing less with each breath, or breathing slowly. We look at our "airflow" channel and interpret these changes as central apneas and hypopneas. We have to resist the temptation to respond to these "events" by increasing CPAP or IPAP or adding a back up rate to the Bilevel. If we slow down and let the body adapt to the new minute ventilation, normal breathing may be restored.

OK, to summarize, increase minute ventilation and the urge to breathe decreases. Decrease minute ventilation and the urge to breathe increases. It is important to understand these concepts so we don't respond to artifactual events that we induced and so we understand the normal response to apneas. As the CO2 increases during the apneas the urge to breath increases, effort increases, and finally the effort is strong enough to get air in. The CO2 is high so breathing increases until the PaCO2 is low enough for normal breathing to resume. Sometimes the increased breathing ("recovery breaths") overshoots and lowers the CO2 too much so a central apnea or hypopnea occurs. When breathing effort starts again, the upper airway is obstructed and the cycle repeats.

If that isn't enough to make one seriously reconsider how we score and respond to "respiratory events" indicated only by changes in temperature (a thermocouple/thermister) and respiratory effort by chest movements without true physiologic measures, listen to this! The instant we fall asleep our control of breathing changes and allows CO2 to build up about 5 mmHg before stimulating a breath. The instant we wake up we sense the higher CO2 and breathe faster to get it back down and our blood pH back to 7.4. So every time one of our patients falls asleep they have a short central apnea or hypopnea to let the CO2 build up and every time they arouse, they breathe faster to get rid of the CO 2. ... in non-REM that is. In REM none of these responses is predictable. All the feedback mechanisms are blunted and breathing becomes irregular. Short central apneas and hypopneas are normal every time there is a sleep onset. Slight hyperventilation is normal with every arousal to wake. Sleep disordered breathing is normal in REM. AND, when we intervene with therapy and change a patient's minute ventilation we can expect to see changes in their breathing patterns that are normal and expected and should not normally be "treated" by responding with changes in therapy. If a patient's cardiovascular system is compromised in some way or lung disease is present, responses to changes in minute ventilation, sleep onset, and REM sleep can be blunted or exaggerated.

If you consider carotid bodies, stretch receptors and other physiologic controls that contribute to the control of breathing, it is easy to see why scoring and responding to respiratory events is as much an art as a science. It also explains why even well educated, experienced technologists and physicians review cases and constantly question and challenge their scoring and treatment intervention decisions. It's only one aspect of a job that is grossly underestimated and should not be left to staff with a week or two of training.

Pamela Minkley RPSGT, RRT
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Title Annotation:SLEEP MEDICINE
Author:Minkley, Pamela
Publication:FOCUS: Journal for Respiratory Care & Sleep Medicine
Date:Mar 22, 2011
Words:1312
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