Respiratory Physiology

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This Chapter on Respiratory Physiology goes into detail on the The Respiratory System including the Structure of the Respiratory System- alveoli, alveolar cells (type I alveolar cells and type II), respiratory and conducting zones and what takes place in each zone. Thoracic Cavity in which the diaphragmn divides into two parts called the Abdominopelvic cavity and the Thoracic Cavity. The abdominopelvic cavity consists of the liver, pancreas, GI tract, spleed, genitourinary tract and other organs, whereas the thoracic cavity consists of the heart, large blood vessels, trachea, esophagus, thymus in the central region and is filled other areas by the right and left lung. It also goes into more depth on the 2 layers of the thoracic cavity ( parietal pleura and visceral pleura). Next, this chapter explains the Physical Aspects of Ventilation; including Intrapulmonary and Intrapleural Pressure and describes Boyle's Law, Physical Properties of the lungs, Surfactant and the Respiratory Distress Syndrome. Then the Mechanics of Breathing that include Inspiration and Expiration, Describes the Pulmonary Function Tests, and Pulmonary disorders such as, Asthma, Emphysema, Chronic Obstructive Pulmonary Disease (COPD), Pulmonary Fibrosis. Next this Chapter goes into Gas Exhange in the Lungs where Calculation of Po2 is discussed, Partial Pressure of Gases in Blood, Significance of Blood Po2 and Pco2 Measurements, Pulmonary Circulation and Ventilation/Prefusion Ratios and lastly discusses the Disorders caused by High Partial Pressures of the Gases which include Oxygen Toxicity, Nitrogen Narcosis, and Decompression sickness. Next Regulation of Breathing is discussed where Brain Stem Respiratory Centers, Effects of Blood Pco2 and pH on Ventilation, Effects of Blood P02 on Ventilation and Effects of Pulmonary Receptors on Ventilation are all discussed. Next is the Hemoglobin and Oxygen Transport where Hemoglobin, The Oxyhemoglobin Dissocciation Curve, Effects of pH and Temperature on Oxygen transport, Effect of 2,3-DPG on Oxygen Transport, Inherited Defects in Hemoglobin Structure and Function and also Muscle Myoglobin is discussed. Carbon Dioxide Transport is also reviewed in this chapter consisting of the Chloride shift and the Reverse Chloride Shift. Acid-Base Balances of the Blood are reviewed and discussed and include Metabolic Acidosis and Alkalosis and also Respiratory Acidosis and Alkalosis. The principles of acid-base balance and also ventilation are in this section of the chapter. The last part of the chapter consists of the Effects of Exercise and High Altitude on Respiratory Function where ventilation is discussed during exercise and also acclimatization to High altitude is described.

Fox, Stuart Ira. (2009). Human Physiology. New York, NY: McGraw-Hill.
PCO2 and pH play a very important role in ventilation. Chemoreceptors make changes to the ventilation so that normal CO2, O2 and pH levels are maintained. Chemoreceptors that are found in the brain have the greatest effects of ventilation. CO2 is monitors very closely because it can cross the blood brain barrier. The rate of ventilation in a healthy person is constantly being adjusted so the PCO2 in arterial blood is kept at about 40 mm Hg. When the CO2 in the blood is inceased the H+ is also increased which will lower the pH in the CSF. When the CSF pH is low the chemoreceptors in the medulla oblongata will be stimulated. However, PO2 levels that are too low will have little to no affect of ventilation. PCO2 and pH are only a small part of ventilation, which is very important to our bodies health.

How is ventilation accomplished?
Ventilation is a process that moves air into the lungs by inspiration and out of the lungs by expiration. There are several muscles in the thoracic and abdominopelvic cavity that aid ventilation. Normal, unforced inspiration primarily uses the diaphragm. It increases the thoracic volume in a vertical direction. The parasternal and external intercostal muscles aid normal inspiration by raising the ribs and increasing thoracic volume laterally. In forced inspiration the scalenes, pectoralis minor and the sternocleidomastic muscles will become involved depending on how forced the inspiration is. These muscles contract to raise the ribs in an anterioposterior direction. Normal expiration is a result of the thorax and lungs recoiling after inspiration making it a passive process. If forced expiration is needed, the internal intercostal muscles contract to depress the ribs. Abdominal muscles also aid in forced expiration by forcing abdominal organs up against the diaphragm decreasing the thoracic volume.


Because the atmospheric pressure is greater than the intrapulmonary pressure air enters the lungs during inspiration. During unforced inspiration the intrapulmonary pressure can decrease 3 mmHg below the atmospheric pressure. For unforced expiration to occur, the intrapulmonary pressure must be greater than the atmospheric pressure. In this case, the inrapulmonary pressure can increase 3 mmHg above the atmospheric pressure. In the intrapleural space (the space between the lungs and chest wall), a subatmospheric pressure called the intrapleural pressure is produced by the opposing elastic recoil of the lungs and chest wall. During inspiration this intrapleural pressure is lower than during expiration, but normally lower than the intrapulmonary pressure during inspiration and expiration. Transpulmonary pressure is the pressure difference across the lung wall. This is the difference between the intrapulmonary and the intrapleural pressures. Intrapulmonary pressure is greater than the intrapleural pressure, this transpulmonary pressure helps to keep the lungs against the chest wall.


The changes in lung volume parallel the changes in the thoracic volume during inspiration and expiration. Boyle's Law states that the pressure of a given quantity of gas is inversely proportional to its volume. This means that an increase in lung volume decreases the intrapulmonary pressure to subatmospheric levels, allowing air to enter the lungs. A decrease in lung volume raises the intrapulmonary pressure to above the level of the atmosphere allowing air to exit the lungs. The changes in lung volume occur because of the changes in the thoracic volume.
The amount of air that is expired in each breath is the tidal volume where the amount of air that can be forcefully exhaled after a maximum inspiration is call the vital capacity. The vital capacity totals the inspiratory reserve, tidal and expiratory reserve volumes together. The expiratory reserve volume is the volume of air left in the lungs after an unforced expiration and the residual volume is the amount of air that cannot be expired after a forced expiration; the sum of these volumes is called the functional residual capacity. During normal unforced breathing, the tidal volume ends at the functional residual capacity allowing the tidal volume inspiration for the next breath start at that level.



The lungs are a complex organ that requires many components to function properly. One important substance people don't always think about is surfactant. Surfactant is a combination of 2 phospholipids phosphatidylcholine and phosphatidylglycerol and hydrophobic surfactant proteins. Surfactant reduces surface tension in alveolar fluids by interspersing itself between the water molecules at the water-air interface which reduces the hydrogen bonds between the water molecules. This makes the surface tension of the alveoli negligible. The lungs maintain a functional level of surfactant by their ability to secrete surfactant into the alveoli through type II alveolar cells and can remove surfactant with alveolar macrophages. During expiration the alveoli get smaller and this improves the ability of surfactant to lower the surface tension as the surfactant molecules become more concentrated. Surfactant prevents the alveoli from collapsing after a full, forceful expiration and allows a residual volume of air to remain in the lungs. Since the alveoli never fully collapse there is less surface tension to overcome as they are inflated during inspiration.

Surfactant is especially important in newborn babies. During fetal life there is no need for the lungs to produce surfactant as the lungs do not breathe air. Toward the end of fetal life the fetus begins producing surfactant in preparation for life outside of the womb. If the baby is born before the surfactant production begins, or before there is sufficient production of surfactant their alveoli can collapse causing respiratory distress syndrome.

Surfactant is also very important to people who develop septic shock. During septic shock inflammation can increase capillary and alveolar permeability which leads to an accumulation of protein-rich fluid in the lungs. This decreases the lung compliance and reduces the amount of surfactant in the alveoli which then further decreases the compliance of the lungs. Together this results in hypoxemia which leads to acute respiratory distress syndrome.


Hemoglobin is a substance located on red blood cells in which oxygen combines. Hemoglobin is made up of 4 polypeptide chains called globins and 4 iron-containing pigment molecules called hemes. Each of the 4 polypeptide chains combine with one heme group. The heme group is a disc-shaped organic pigment molecule in which the center is an atom of iron which is able to combine with 1 oxygen molecule. Since each heme group can combine with 1 oxygen molecule and there are 4 heme groups each hemoglobin molecule can combine with 4 oxygen molecules. Each red blood cell has about 280 million hemoglobin molecules so each red blood cell can therefore carry over a billion molecules of oxygen. Heme normally contains a reduced form of iron which is ferrous iron of Fe2+. As Fe2+ the iron can bond with oxygen by sharing electrons to the hemoglobin forms oxyhemoglobin. When the oxyhemoglobin dissociates to release oxygen to the tissues the hemoglobin is considered deoxyhemoglobin as it isn't carrying oxygen.

An abnormal form of hemoglobin in the blood is known as carboxyhemoglobin. Carboxyhemoglobin is when the Fe2+ combines with carbon monoxide instead of oxygen. Since carbon monoxide forms a bond 210 times stronger than the bond it has with oxygen the oxygen is displaced and remains attached to the hemoglobin as it passes through the capillaries. This reduces the transport of oxygen to the tissues and is known as carbon monoxide poisoning.

The percent oxyhemoglobin saturation of the blood is measured to determine the oxygenation level of the blood. The normal saturation level is 97%. If the blood is properly saturated with oxyhemoglobin the blood will be a bright red color. If the blood is more concentrated with carboxyhemoglobin it is a less red color like cranberry juice. The percent of saturation can be easily measured with a pulse oximeter or with a blood sample can be measured with a blood-gas machine.

Ventilation and pH balance

The pH of the blood is a complicated balance divided into the respiratory component and the metabolic component. The respiratory component of blood pH is determined by the carbon dioxide concentration of the blood and is measured by PCO2. Under normal conditions the ventilation is adjusted to keep pace with the metabolic rate therefore the PCO2 remains in a normal range. If ventilation is insufficient and the body is not removing enough carbon dioxide as in hypoventilation the PCO2 of the blood is high and respiratory acidosis occurs. If ventilation is high as in hyperventilation PCO2 levels decrease raising the pH of the blood causing respiratory alkalosis. If the metabolic component of pH balance is off the respiratory component can work to compensate for the change. If a person goes into metabolic acidosis the person will hyperventilate. The hyperventilation causes a secondary respiratory alkalosis to occur. The person would still have acidosis but the respiratory compensation helps to raise the blood pH and raise the PCO2.

Fox, Stuart Ira. (2009). Human Physiology. New York, NY: McGraw-Hill.

As a nurse, I will need to know how to identify the normal breathing sounds of the lungs along with the normal breathing rate. If a patient comes in who is having difficulties breathing or is short of breath I will need to be able to identify possible causes and treatments to be able to help the patient be able to breath more easily.One example may be if a patient (who is a chronic smoker) comes in with chest pains and unable to catch his breath and having coughing fits, I might look at an x-ray of his lungs and find that he has Emphysema. In this case the patient was diagnosed early and an inhaler may be prescribed and information on quitting smoking may be given to the patient.

CASE STUDY: Into Thin Air

  1. What types of physiological problems do humans encounter at high altitudes? Physiological problems humans encounter at high altitudes until they become acclimated include headaches, shortness of breath, fatigue, anorexia, interrupted sleep, and general malaise. In altitudes above 9,000 feet, pulmonary edema is common and cerebral edema at altitudes of 10,000 feet may produce mental confusion and hallucinations.
  2. What symptoms did the climbers exhibit that might be related to altitude? Explain. The climbers exhibited labored breathing, exhaustion, and a headache. The labored breathing, exhaustion, and headache may be a direct result of the decreased P02 at the higher altitude. At higher altitudes, the amount of oxygen able to attach itself to hemoglobin decreases, causing the O2 content of blood to decrease. The hypoxemia will cause fatigue (exhaustion) because the cells in the body aren't getting the oxygen they need to function. The labored breathing is caused due to the carotid bodies in the aortic arch recognizing the decrease in arterial P02, and attempting to get more oxygen to the body's cells. Unfortunately, this hyperventilation can't increase blood P02 above that of inspired air. The headache may result due to vasodilation (caused by the low arterial P02) of blood vessels in the brain, increasing the pressure within the skull.

  3. Compare the air at 18,000 feet (atmospheric pressure 280 mm Hg) to the air at sea level (760 mm Hg). What specific changes in the primary atmospheric gases (nitrogen, oxygen, carbon dioxide) might occur? Are they significant? The air at sea level contains approximately: P02 in air(mmHg)=159; P02 in alveoli (mmHg)=105; P02 in arterial blood (mmHg)=38%. The air at 18,000 feet is approximately: P02 in air (mmHg)=75; P02 in alveoli (mmHg)=42; P02 in arterial blood (mmHg)=38%. Primary atmospheric gases at sea level are: 21% oxygen, 78% nitrogen, and 1% other gases. Primary atmospheric gases are the same at 18,000 feet, but, as the altitude increases, the atmospheric pressure decreases. This means that because of the decrease in atmospheric pressure, the air molecules are more dispersed than they would be at sea level, causing less oxygen to be delivered to the body during inspiration.
  4. What is the specific pulmonary response to high altitude? [Assume you are considering a subject at rest.] Due to a decrease in oxygen at high altitudes, oxygen sensing cells in the carotid body will increase ventilation as the amount of oxygen in the arterial blood decreases, causing hyperventilation. This hyperventilation increases alveolar P02.
  5. How will this response affect overall blood gases? What about oxygen loading and unloading from hemoglobin? Explain how you arrived at your conclusions. The hyperventilation response due to the decreased oxygen in the blood causes a decrease in PC02, which will cause a condition known as respiratory alkalosis. Respiratory alkalosis is when the pH of the blood is high, the PC02 is low, and the person will experience rapid breathing (hyperventilation). This respiratory alkalosis causes the hemoglobin in the blood to have a greater affinity to oxygen; so more oxygen (due to the hemoglobin) is loaded in the lungs.
  6. After breathing at altitude for a few days, the body normally begins producing more 2,3-DPG. What is the significance of this change? How will it affect the pulmonary changes observed? 2,3-DPG is produced by RBC's due to low oxyhemoglobin, which in turn will lessen hemoglobin attachment to oxygen and give it to the body tissues. Production of 2,3-DPG increases when there is less oxygen getting to the body tissues, such as hypoxemia (as in this case study) and the body needs more oxygen. Hence, more 2,3-DPG production, the more oxygen is delivered to the body tissues. The person will be less exhausted (fatigued), headaches will lessen due to oxygen being given to the peripheral tissues and breathing will become more normal (not labored and not hyperventilating).

  1. What physiological changes is Emily referring to (above) that will occur when someone lives at altitude for an extended period? Physiological changes are the body's ability to adapt to the decrease in atmospheric pressure and the body's increase production of 2,3-DPG.
  2. How are these changes advantageous? These physiological changes are advantageous because it allowed them to get enough oxygen in their body's tissues to maintain homeostasis, and not have adverse side effects like the other hiker is now experiencing due to having not conditioning his body properly.
  3. What is the specific physiological pathway that results in the changes described. After a few day at a increased elevation, the body's RBC's will produce 2,3-DPG, which will increase the affinity of hemoglobin to oxygen. This affinity will get the tissues of the body the oxygen it needs. After a few weeks, when the kidneys detect a chronically low oxygen level (hypoxemia), it will secrete a hormone called erythropoietin. Erythropoietin stimulates RBC production in the bone marrow, which will increase the number of RBC's and hemoglobin, thus increasing oxygen amount in the blood.
  4. How would the oxygen and Gammow bag help Mark? A Gammow bag is a cylindrical inflatable pressure bag designed to fit an adult body inside it. It is essentially a portable hyperbaric chamber which can stimulate conditions at lower altitudes, thus, increasing the atmospheric pressure and help our victim breathe easier. Oxygen would help by giving the body the extra oxygen it is wanting to increase blood O2 and allow his body to disperse it to the peripheral tissues to maintain metabolic processes and maintain homeostasis.High Altitude Mountain Rescue 101
  5. If you were a member of the medical team examining Mark, what types of tests would you run? Why? [Try to focus on what types of things you would like to measure, whether or not you know of a possible test for them.] I would run a hematocrit test to see how many RBC's he has in his lodd which will let us know if he would be able to maintain proper a oxygenation level at the higher elevation. I would also like to know how much oxygen is in his blood (arterial blood) to see if his body was low on oxygen. I would also check his blood pH. Since I know he had respiratory alkalosis due to hyperventilation, I would like to know how his body's (metabolic) reaction was.
  6. What types of results do you expect to find? Explain your reasoning. Hematocrit level I expect to see levels around that of an individual at sea level because he was not on the mountain long enough to make more RBC's. Arterial oxygen I would expect to be lower than normal because of the fact he was having difficulty breathing and his body was in need of oxygen. Arterial pH (metabolic) I would expect to be low because a person with metabolic acidosis will hyperventilate due to the carotid/aortic bodies recognizing the increase in H+ in the blood. As a result of the metabolic acidosis, the body tries to compensate and respiratory alkalosis will occur (which I know he experienced).
  7. Are the results as you expected? What values agree/disagree with your predictions? Yes and no. The arterial oxygen amount in his blood was less than normal like I predicted, as was his arterial pH. His hematocrit level, however, was surprisingly higher than normal.
  8. Which lab values appear to represent the most serious problem Mark is having? Is his situation life-threatening? The most serious problem Mark is having is his arterial oxygen amount. This is a very life threatening situation because if his body does not get the oxygen it needs and quickly, permanent death of his body's cells may occur.
  9. Compare the results of Alveolar Oxygen Tension to Arterial Oxygen levels. What might cause this type of discrepancy? Mark's alveolar oxygen tension was 110 Torr compared to the normal average of 98-104 Torr. Mark's arterial oxygen was 52 compared to the normal average of 80-100 Torr. Mark's body did not have enough RBC's (with hemoglobin attached) to collect the oxygen in his alveoli and distribute it to his body, so his arterial 02 was low because it wasn't getting the oxygen it wanted. His body tried to compensate for this lack of oxygen by hyperventilating to get more oxygen into his body (thus, increasing alveolar oxygen level), but, due to the lack of RBC's could not deliver that extra O2 to his body's cells.
  10. Overall, what do these findings tell you about possible diagnoses for Mark's condition? I would have to say that after reading in my textbook, he may have pulmonary edema. He had a headache, cough, shortness of breath, fatigue, and the fact that the alveoli in his lungs had excess oxygen, but, it was not getting to his body's cells as evidenced by his low arterial blood oxygen level.