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The Physiology of Respiration
This CE activity is approved by EMS World Magazine, an organization accredited by the Continuing Education Coordinating Board for Emergency Medical Services (CECBEMS) for 1 CEU. To take the CE test that accompanies this article, go to www.rapidce.com to take the test and immediately receive your CE credit. Questions? E-mail editor@EMSWorld.com.
EMS providers are often summoned to assist patients in respiratory distress. The subjective sensation of difficulty breathing—known as dyspnea—experienced by these patients can be caused by myriad conditions.1 The causes range from non-life-threatening conditions (e.g., a muscle strain causing pain on inspiration), to complex mixed medical conditions that lead to confusing patient presentations (e.g., acute cardiogenic pulmonary edema and pneumonia).
It can sometimes be difficult to discern the root cause of a patient’s condition with the limited diagnostic resources available to EMS. Some providers may focus on differentiating between specific diagnoses, while others may offer the same treatment to all patients who verbalize a complaint of difficulty breathing. As EMS providers, we need to be better prepared to isolate the specific difficulty a patient is experiencing when they complain of difficulty breathing (e.g., getting air in/getting air out and inadequate gas exchange). Hopefully, with a broader knowledge of respiratory physiology, you will be able to recognize the specific area of compromise, which will guide you to the appropriate intervention.
Overview of Respiration
Taber’s Cyclopedic Medical Dictionary defines respiration as the “interchange of gases between an organism and the medium in which it lives.”2 In the human body, we can further classify respiration by external and internal processes.3 The external process of respiration involves the transfer of oxygen (O2) and carbon dioxide (CO2) that occurs in the lungs between the atmosphere and the pulmonary circulation. The internal process of respiration is the similar process that occurs at the cellular level. While both aspects of respiration are essential to life, this article focuses on external respiration and its three primary components: ventilation, perfusion and diffusion. A thorough understanding of each of these components and their potential impairments can guide EMS providers in their efforts to manage patients who complain of difficulty breathing.
The Respiratory System (Physiology)
The ultimate function of the respiratory system is gas exchange.4 This gas exchange consists of obtaining O2 from the atmosphere and removing CO2 from the blood. It is important to consider that O2 is necessary for normal metabolism and CO2 is a waste product of this metabolism. CO2 is only inhaled in negligible quantity and thus the CO2 we exhale is created within the body. While CO2 plays a role in acid-base balance, it must be cleared from the body in appropriate levels through ventilation.
Neural Control of Respiration
Although gas exchange takes place in the lungs, the respiratory system is controlled by the central nervous system (CNS).4 While we do have some voluntary control of breathing, it is regulated automatically and functions whether we think about it or not. Breathing can, however, be suppressed at the neurological level due to narcotic or sedative overdose, as well as brainstem injury.4
The portions of the CNS that control respiration are located within the brain stem—specifically within the pons and the medulla. These components are responsible for the nerve impulses, which are transmitted via the phrenic and other motor nerves to the diaphragm and intercostal muscles, controlling our basic breathing rhythm. Also located in the brainstem are the central chemoreceptors. These specialized cells signal the body to adjust ventilation based indirectly on arterial CO2 (PaCO2) levels. This accounts for our primary respiratory drive. The peripheral chemoreceptors, which are located outside of the brainstem in the carotid and aortic arteries, serve as the body’s back-up respiratory drive by responding to low levels of O2. This secondary mechanism is often referred to in COPD patients as a “hypoxic drive” since it takes over as the primary respiratory stimulation after the central chemoreceptors grow numb to chronically elevated PaCO2.
Ventilation
The most readily observable component of respiration involves the act of breathing, “during which the lungs are provided with air through inhaling and CO2 is removed through exhalation.”2 This process of moving air into and out of the lungs is known as ventilation.1 While it may seem a simplistic process, the ability of air to flow into and out of the alveoli is dependent on a number of factors including integrity and compliance of the lung tissue and resistance to airflow within the airways.3
Approximately 10 –12 times per minute in an adult, the diaphragm and thoracic muscles receive impulses from the brain signaling them to contract. This contraction moves the diaphragm downward and the rib cage up and out, which increases the volume of the thoracic cavity and creates a negative pressure within the lungs. This causes air from the higher-pressure environment outside the body to flow into the lower-pressure environment in the lungs. This is the active phase of ventilation, known as inhalation.4 Air continues flowing through the airway openings and into the lungs while equalization of pressure occurs.5 After full expansion of the lungs, stretch receptors signal the brainstem and inhalation ceases. The passive phase of ventilation, known as exhalation, then begins. The diaphragm and thoracic muscles relax and the lungs recoil, which decreases the volume and increases the pressure in the thoracic cavity. The air inside the lungs then flows back out to the lower-pressure atmosphere outside of the body.4 Since exhalation is a passive process, it typically takes twice as long as the active process of inhalation.3
Through this process of inhalation and exhalation, the average human cycles 5 to 10 liters of air through the lungs each minute.3 The amount of air taken into the lungs during each breath (approximately 500 mL in an adult) is known as tidal volume (VT), while the collective volume over the course of a minute (respiratory rate x VT) is known as the minute volume (VE). Due to the lack of gas exchange that occurs in the conducting airways (from the mouth to the terminal bronchioles), a portion of each breath is ineffective for gas exchange. This anatomical dead space (VD) is approximately 150 mL in the average adult and must be subtracted from the VT in order to determine the volume of air that reaches the alveoli (VA), and can be used for gas exchange. Table I shows how VA is affected by variations in respiratory rate and VT. While the EMS provider will not measure these volumes, it is important to understand the underlying concept.
As previously noted, CO2 is created within the body and it is the role of ventilation to rid the body of this waste product. It is also for this reason that ventilation is best evaluated through a measure of CO2 (PaCO2 or PETCO2).1 If breathing stops (apnea) or if the VE decreases (hypoventilation), CO2 will accumulate within the blood and rapidly reach toxic levels (hypercapnea), resulting in acidosis. Conversely, if VE increases (hyperventilation), the excessive elimination of CO2 (hypocapnea) will result in alkalosis. It is in this manner that our respiratory system affects the body’s pH and can also serve as a compensatory mechanism to offset metabolic derangements.
Perfusion
The second component of respiration is perfusion. This process involves the circulation of blood through the capillaries, which facilitates nutrient exchange.6 External respiration requires adequate delivery of blood to the capillary beds of the lungs via the pulmonary circulation. In the absence of this blood supply, there will be no transport mechanism for O2.3
Diffusion
Diffusion is another important method of transport within the body and is the third component of respiration. Diffusion involves the movement of a substance in a solution (liquid or air) from higher concentration areas to lower concentration areas.7 In the case of respiration, diffusion involves the distribution of O2 from the atmosphere through the pulmonary capillary walls and into the bloodstream. At the same time, CO2 diffuses from the bloodstream into the alveoli. This process of diffusion is dependent on the characteristics of each individual gas, the rate of perfusion and the integrity of the alveolar-capillary membrane.1
Most EMS providers are familiar with the fact that our atmosphere contains approximately 21% O2. At sea level, under normal conditions, barometric (i.e. atmospheric) pressure is 760 mm Hg. According to Dalton’s law, this pressure is comprised of the partial pressures of the individual gases that make up our atmosphere: primarily nitrogen (N2) and O2.3 In this situation, the partial pressure of O2 is 159 mm Hg (21% of 760 mm Hg). By the time O2 diffuses into the human circulation, its partial pressure (PaO2) is reduced to 80–100 mmHg.1 While the percentage of O2 making up our atmosphere remains constant, we can enhance the process of diffusion through a combination of supplemental O2 and altering the airway pressure (e.g., CPAP) or by altering a combination of barometric pressure and O2 concentration (e.g., hyperbaric chamber).
Impairment of Effective Respiration (Pathophysiology)
In the healthy individual, the breathing cycle is silent, automatic and effortless.4 Many disease states affect the respiratory system and interfere with its ability to acquire the O2 and nutrients required for normal cellular metabolism. Others limit the body’s ability to get rid of waste products such as CO2.6 Any disease process that impairs the respiratory system will ultimately result in a disruption in ventilation, diffusion and perfusion, or any combination of these processes.6 Our understanding of the normal variances of these processes will assist in our recognition of these disease processes and direct us toward the appropriate corrective actions.
Disruption in Ventilation
Disruption in ventilation is the most common respiratory complication we encounter in the field. Luckily, it is the easiest to intervene against using BLS maneuvers.6 Diseases that affect ventilation result in restriction or obstruction of the normal conducting airways, as well as impairment of the chest wall. Other disruptions in ventilation are caused by impairment of the chest wall, abnormalities involving the nervous system’s control over ventilation and metabolic derangements that require respiratory compensation.6
In an ideal world, the ventilation and capillary blood flow to each section of the lung, known as the ventilation-perfusion ratio (V/Q ratio), would be equal.3 Alterations in the V/Q ratio create a condition known as V/Q mismatch. In situations where a portion of the lungs is not ventilated (e.g., atelectasis), the blood flow through the pulmonary capillary circulation is unable toreceive O2 and unload CO2, thus creating a decreased V/Q ratio (i.e. more pulmonary capillary blood flow than ventilation). This form of V/Q mismatch is referred to as a pulmonary shunt.3
Disease states that affect the upper respiratory tract restrict ventilation to the structures of the lower respiratory tract. Examples of upper airway obstructions include: foreign bodies, upper airway trauma, infections (e.g., epiglottitis) and formation of abscesses within the pharynx.6 These complications are classified as restrictive disorders.
The lower respiratory tract may be obstructed by trauma as well, but is more commonly offended by inflammation, aspiration, excessive mucus accumulation or smooth muscle constriction (bronchoconstriction). The lower airways can also be affected by edema secondary to infection or burns.6 Conditions of the lower airways (e.g., bronchospasm) often inhibit CO2 clearance and are referred to as obstructive disorders.
Impairment of the chest wall can result from chronic (e.g., kyphosis, scoliosis, obesity) or acute (e.g. trauma, infection) causes. Injuries to the chest wall, such as pneumothorax and hemothorax, can disrupt the normal mechanics of ventilation by causing a loss of negative pressure within the pleural space.5,6 Chest wall injuries can also inhibit full expansion of the pleural cavities as in diaphragmatic hernia and flail chest.6
Neuromuscular diseases such as spinal cord trauma, tetanus, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS) and myasthenia gravis can also inhibit ventilation.6 These conditions may inhibit diaphragmatic and chest wall function and often reduce a patient’s ability to clear secretions. Diseases affecting the interstitium of the lungs can decrease compliance (i.e., elastance) and thus inhibit inhalation. Most of these conditions are permanent and progressive, yet some (e.g., myasthenia gravis) can be episodic.
Disruption in Diffusion
Disruption of the diffusion of gases within the lungs can occur as a result of disease or an altered pressure gradient. The most common cause of disruption of diffusion is thickening of the alveolar-capillary membrane as seen with pulmonary edema.6 This is commonly seen in patients with left-sided heart failure and is due to increased venous pressure, which can result from a poor functioning left ventricle. Similarly, changes in the permeability of the alveolar-capillary membrane, as with the release of histamine, can lead to fluid accumulation within the interstitial spaces of the lungs resulting in an inflammation of the pleural tissue, or more severely, adult respiratory distress syndrome (ARDS).6 These conditions will likely require some form of positive pressure ventilation.
Disruption in Perfusion
Hemoglobin is the component of the blood that transports O2. It also plays a significant role in the elimination of CO2. Any alteration in adequate blood flow through the pulmonary circulation will therefore limit normal gas exchange.6 Such alterations will result in an increased V/Q ratio (i.e., more ventilation than pulmonary capillary blood flow). This form of V/Q mismatch is referred to as dead-space ventilation.8
Diseases that limit circulating blood volume or inhibit the flow of blood through the pulmonary circulation include shock, hemorrhage and dehydration.6 In patients whom experience pulmonary embolism, the blockage of a division of the pulmonary artery prevents perfusion of the lung segments distal to the obstruction. As a result, ventilation to the affected lung segments is wasted, and de-oxygenated blood is returned to the heart via the pulmonary circulation.
Assessment
As with any patient, should first look for and intervene against immediate life threats. Your assessment should then include a history and physical exam. The process of gathering a history from the respiratory patient should utilize the standard pneumonics OPQRST and SAMPLE.9 Pay particular attention to details of the patient’s past medical history, current medications and onset of current conditions, as these will often yield vital information to aid in identifying the current source of their respiratory compromise.
Physical Exam
Speak to the patient at the first opportunity, as this will provide you information about the patient’s mental status and ability to ventilate. As soon as you are able to visualize the patient, pay attention to the patient’s position and work of breathing. Look not only at the presence of accessory muscle use, but also at which accessory muscles the patient is using (see Figure 1). During times of distress, additional muscles are recruited to assist in either inhalation or exhalation.3 Identifying which of these muscles a patient is using can help differentiate between restrictive and obstructive conditions (see Table II). Additional signs that can be detected by inspection (e.g., barrel chest and clubbed fingers), can tell you about a patient’s history, but do not assume that history is the cause of the patient’s current distress. The acute onset of a different condition may be to blame.
Prior to auscultating the patient’s breath sounds, place your hands on the patient’s chest and feel for equal expansion. At the same time make note of the patient’s skin color, temperature and condition over their core. This might be different than the peripheral findings you encountered when initially checking the patient’s radial pulse. Unequal expansion of the patient’s chest could suggest a lack of ventilation on the affected side, which could be causing a pulmonary shunt. An appreciable lack of bilateral expansion is suggestive of a restrictive disorder or chest wall impairment, in which case it may be necessary to assist the patient with positive pressure ventilation. Hyperinflation of the chest on one side, with paradoxical rise and fall, should raise suspicion of a pneumothorax. Evaluate the patient’s hemodynamic status and intervene per your local protocol. Bilateral hyperinflation indicates a potential obstructive disorder with air trapping and the possible need for a bronchodilator.
While some sources might suggest the use of palpation as the next step in your assessment, it can be difficult to appreciate delicate acoustics in the prehospital environment.9 The same can be said for auscultation. While auscultation is not a step you should skip, do not get caught up in the battle of rales versus rhonchi. Both of these sounds describe fluid of varying viscosity within the airways, and since you were probably exposed to loud noises enroute to the call (i.e., your partner’s preferred wail/yelp pattern), it’s quite possible that your sense of hearing has been dulled.10 Regardless, these breath sounds, which we’ll generically refer to as crackles, can more accurately be described as fine or coarse, inspiratory or expiratory, and by their location. Wheezes are unique in their high-pitched musical sound and are not likely to be confused with crackles. Wheezes are indicative of bronchospasm and typically indicate the need for bronchodilators. However, bronchospasm might be associated with underlying pulmonary edema (i.e., cardiac wheezes). Some argue against the administration of bronchodilators in these cases out of fear of increasing the cardiac workload;11 however, it can also be argued that the use of CPAP (an essential therapy in the treatment of pulmonary edema) can result in barotrauma if used in the presence of increased airway resistance associated with bronchospasm. It is advisable to use any additional diagnostic tools at your disposal to aid in your determination of the patient’s specific respiratory compromise, and follow your local treatment protocols to intervene against any respiratory disruptions you detect.
Assessment Tools
In addition to the physical assessment, there are two primary tools that EMS providers can use to assess a patient’s respiratory status: pulse oximetry (SpO2) and capnography (PETCO2). It is essential that the clinician obtain both SpO2 and PETCO2 measurements in the respiratory patient in order to distinguish between disruptions in oxygenation and ventilation, or to identify disruptions of both. Identification of the specific area of compromise can guide the EMS provider toward appropriate intervention.
SpO2 measurements are gathered with the use of a pulse oximeter, which passes two wavelengths of light through a patient’s tissue (e.g., finger or earlobe) in order to estimate the percentage of arterial hemoglobin bound with O2.1 There has been recent debate on what an appropriate SpO2 reading should be and science is finally beginning to over-run EMS anecdote regarding the administration of supplemental oxygen. The American Heart Association now recommends the titration of supplemental oxygen to achieve a SpO2 of ≥ 94%. In situations where a pulse oximeter is not available, it is acceptable to proceed with supplemental oxygen. The lack of science to support the wide spread use of supplemental oxygen, as well as the recognition of the potential dangers of hyperoxia, are the driving forces behind these changes. Even with shorter durations of administration, high-flow O2 can result in a thickening of the alveolar-capillary membrane, substernal chest pain and the proliferation of free radicals.1 Further, the wash out of N2 can cause a condition known as absorption atelectasis, which causes the alveoli to collapse. This condition can prevent the further ventilation of the effected lung section until positive pressure is applied.1
Regardless of these recent findings, old habits die hard. It is still commonplace for EMS providers to administer supplemental oxygen to a patient who complains of difficulty breathing yet shows 100% oxygen saturation. While it is certainly good advice to “treat the patient and not the monitor,” it is also a good idea to consider the presence or absence of physical signs indicating hypoxia (e.g., cyanosis, irritability). It is important to recognize that a patient who is complaining of difficulty breathing but is oxygenating, likely has a disruption in another aspect of respiration (e.g., ventilation), rather than a problem with oxygenation. Be sure to consider other possible causes (e.g., increased CO2 production leading to fatigue) rather than providing oxygen to a patient who does not need it.
While SpO2 is essentially a measure of oxygenation, PETCO2 provides a measure of ventilation.12 PETCO2 measurements can include continuous waveforms in addition to quantitative values. These readings can be obtained through an inline circuit for an intubated patient or with a nasal cannula style circuits for non-intubated patients. When evaluating PETCO2 values, readings greater than 45 mm Hg indicate hypoventilation, while readings below 35 mm Hg suggest hyperventilation. Such readings that persist despite intervention are suggestive of an underlying metabolic or neurological disorder. Evaluation of the capnography waveform, if available, can provide clues to conditions such as bronchospasm and pulmonary emboli.1 While a thorough lesson on PETCO2 waveform analysis is beyond the scope of this article, there are many resources available to gain knowledge on this topic.
While these assessment tools have been widely accepted, they are not without limitations. Always confirm the accuracy of the pulse reading prior to accepting a SpO2 reading as valid.9 Also verify the presence of a pulsatile component (e.g., waveform) when available, as this will also verify perfusion of the tissue at the monitoring site.1 Factors that reduce the accuracy of SpO2 readings include patient exposure to carbon monoxide, dark nail polish or skin pigment, motion, ambient light and poor perfusion. It is also important to consider that a patient must have adequate levels of hemoglobin in order for a SpO2 value to have merit. Patients with anemia (e.g., blood loss) may present with high saturation levels despite being hypoxic.
Conclusion
EMS providers are often challenged by the varying presentations of patients who complain of difficulty breathing. It is important that we focus greater attention on the specific cause of our patient’s respiratory problem as it relates to the three principles of respiration: ventilation, perfusion and diffusion. By applying an understanding of these principles to our assessment process, we can pick up on clues that might otherwise be missed. Once we detect the specific type of impairment our patient is experiencing, we will be able to tailor our intervention using the most appropriate treatment regimen.
References
1. Wilkins RL, Stoller JK, Kacmarek RM. Egan’s Fundamentals of Respiratory Care 9th ed. St. Louis, MO: Mosby, 2009.
2. Venes D (Ed). Taber’s Cyclopedic Medical Dictionary 21st ed. Philadelphia, PA: F.A. Davis Company, 2009.
3. Des Jardins T. Cardiopulmonary Anatomy & Physiology: Essentials of Respiratory Care 5th ed. Clifton Park, NY: Delmar, 2008.
4. Martin L. Breathe Easy A Guide to Lung and Respiratory Diseases for Patients and Their Families. www.lakesidepress.com/pulmonary/books/breathe/.
5. Campbell JE (Ed). International Trauma Life Support for Prehospital Care Providers 6th ed. Upper Saddle River, NJ: Pearson Education, 2008.
6. Bledsoe BE, Porter RS, Cherry RA. Essentials of Paramedic Care 2nd ed. Upper Saddle River, NJ: Prentice Hall, 2006.
7. Shier D, Butler J, Lewis R. Hole’s Human Anatomy & Physiology 10th ed. New York, NY: McGraw-Hill, 2009.
8. Koschel M J. Pulmonary embolism. Am J Nurs 104:46–50, 2004.
9. Dalton AL, Limmer D, Mistovich JJ, Werman HA. Advanced Medical Life Support 3rd ed. Upper Saddle River, NJ: Pearson Education, 2007.
10. Fernandez AR, Crawford JM, Studnek JR, Wilkins JR Hearing problems among a cohort of nationally certified EMS professionals. Am J of Ind Med 53: 264–275, 2010.
11. Singer AJ, Emerman C, Char DM, Heywood JT, et al. Bronchodilator therapy in acute decompensated heart failure patients without a history of chronic obstructive pulmonary disease. Ann Emerg Med 51(1), 25–34, 2008.
12. Murphy MF. Pulse Oximetry. In Walls RM, Murphy MF, Luten RC, Schneider RE (Eds.). Manual of Emergency Airway Management 2nd ed. Philadelphia, PA: Lippincott, Williams, & Wilkins, 2004.
Elliot Carhart is an EdD candidate at Nova Southeastern University where his studies have focused on healthcare education. He is a firefighter/paramedic with the Pinellas Park (FL) Fire Department and is an adjunct faculty member in the College of Health Sciences at St. Petersburg College. He is also a registered respiratory therapist. Contact him at carhart.elliot@gmail.com.
Comments
Article is very informative and well written. I appreciate the "do not get caught up in the battle of rales versus rhonchi" admonishment as it is important to recognize and treat the problem of fluid in the airways.
—Frank Wall