Respiratory Physiology

Unit Overview:
The primary function of the respiratory system is to supply the blood with oxygen in order for the blood to deliver oxygen to all parts of the body. The respiratory system does this through breathing. When we breathe, we inhale oxygen and exhale carbon dioxide. This exchange of gases is the respiratory system's means of getting oxygen to the blood. Respiration is achieved through the mouth, nose, trachea, lungs, and diaphragm. Oxygen enters the respiratory system through the mouth and the nose. The oxygen then passes through the larynx (where speech sounds are produced) and the trachea which is a tube that enters the chest cavity. In the chest cavity, the trachea splits into two smaller tubes called the bronchi. Each bronchus then divides again forming the bronchial tubes. The bronchial tubes lead directly into the lungs where they divide into many smaller tubes which connect to tiny sacs called alveoli. The average adult's lungs contain about 600 million of these spongy, air-filled sacs that are surrounded by capillaries. The inhaled oxygen passes into the alveoli and then diffuses through the capillaries into the arterial blood. When this happens, the waste-rich blood from the veins releases its carbon dioxide into the alveoli. The carbon dioxide follows the same path out of the lungs when you exhale. The diaphragm's job is to help pump the carbon dioxide out of the lungs and pull the oxygen into the lungs. The diaphragm is a sheet of muscles that lies across the bottom of the chest cavity. As the diaphragm contracts and relaxes, breathing takes place. When the diaphragm contracts, oxygen is pulled into the lungs. When the diaphragm relaxes, carbon dioxide is pumped out of the lungs.

1. The Respiratory System & Physical Aspects of Ventilation

The Respiratory System

Respiration includes 3 related functions:

I. Ventilation (breathing)
II. Gas Exchange, which occurs between the air and blood in the lungs and between the blood and other tissues of the body
III. Oxygen Utilization (cellular respiration)

Ventilation moves air in and out of lungs for gas exchange with blood (external respiration.) Gas exchange between blood and tissues, and O2 use by tissues is internal respiration. Gas exchange is passive via diffusion- cellular respiration (moving from high to low.)

Alveoli are microscopic thin-walled air sacs that provide an enormous surface area for gas diffusion.

Air passes from the mouth or nose to the Larnyx to the Trachea, then the Right and Left Bronchi to Bronchioles to the Terminal Bronchioles to the the Respiratory Bronchioles to the Alveoli.

The region of the lungs where gas exchange with the blood occurs only in the respiratory bronchioles and alveoli is known as the respiratory zone. The Trachea (windpipe), Bronchi, and Bronchioles that deliver air to the respiratory zone comprising all other structures which makes up the conducting zone: Warms and humidifies inspired air. Mucus lining filters and cleans inspired air, Mucus moved by cilia will be expectorated or to remove dust and other particles out of the lungs.

Gas Exchange occurs across the 300 million alveoli (60-80 m2 total surface area) Only 2 thin cells are between lung air and blood: 1 alveolar and 1 endothelial cell.

Type I alveolar cells- creates the air sac

Type II alveolar cells- secretes surfactant and absorbs sodium and water

The thoracic cavity is limited by the chest wall and diaphragm.

The structures of the thoracic cavity are covered by thin, wet pleural membranes. The lungs are covered by a visceral pleura that is normally flush against the parietal pleura that lines the chest wall. The potential space between the visceral and parietal pleurae is called the intrapleural space they expand and contract with the thoracic cavity. It is created by the diaphragm, a dome-shaped sheet of skeletal muscle. The cavity also contains the heart, large blood vessels, the trachea, esophagus, thymus, and lungs. Below the diaphragm is the abdominopelvic cavity which contains the liver, pancreas, GI tract, spleen, and genitourinary tract.

Physical Aspects of Ventilation

Ventilation comes from pressure differences induced by changes in lung volumes. Air moves from higher to lower pressure and compliance, elasticity, and surface tension of the lungs influence the ease of ventilation.

The intrapleural and intrapulmonary pressures vary during ventilation.
  • The Intrapleural pressure is outside the lungs in between the pleuras.
  • The Intrapulmonary pressure is within the lungs.

The intrapleural pressure is always less than the intrapulmonary pressure.

The intrapulmonary pressure is subatmospheric or about -3mmHg during inspiration and greater than the atmospheric pressure or about +3 mmHg during expiration.

Positive transmural pressure= intrapulmonary - intrapleural pressures, keeps the lungs inflated at all times. If there is a puncture in the lungs it will change the pressure, which will deflate the lung causing a major breathing problem when this happens it is known as a clasped lung.

Pressure changes in the lungs are produced by variations in lung volume, in accordance with the inverse relationship between the volume and pressure of a gas described by Boyle’s Law.

Boyle's Law implies that changes in the intrapulmonary pressure occurs as a result of changes in lung volume. The pressure of gas is inversely proportional to volume. Example as the volume of the lungs increase the pressure of the lungs will decrease during inhalation. When the volume of the lungs decrease then the pressure of the lungs will increase during exhalation.

The mechanics of ventilation are influenced by the physical properties of the lungs.

The compliance of the lungs, or how ease the lungs expand with pressure, refers specifically to the change in lung volume per change in transpulmonary pressure (the difference between intrapulmonary pressure and intrapleural pressure). It can be reduced by factors that causes resistance to distension or its stretchability an example of this kind of resistance is Pulmonary Fibrosis.

The elasticity of the lungs refers to their tendency to recoil to their initial size after distension. This is do to the high content of elastin proteins in the lung tissue. Elastic tension increases during inspiration and is reduced by recoil during expiration.

Surface Tension

The surface tension of the fluid in the alveoli exerts a force directed inward or collapse, which acts to resist distension.
The lungs secrete and absorb fluid, normally leaving a thin film of fluid on alveolar surfaces. The fluid absorption occurs by osmosis driven by Na+ active transport or Alveoli II cells. Fluid secretion is driven by active transport of Cl- out of alveolar epithelial cells. This film causes surface tension because water molecules are attracted to other water molecules. On first consideration, it would seems that the surface tension in the alveoli would create a pressure that would cause small alveoli to collapse and empty their air into larger alveoli. This would occur because the pressure caused by a given amount of surface tension would be greater in smaller alveoli than in large alveoli, as described by the Law of LaPlace.

Law of LaPlace states that pressure in the alveolus is directly proportional to surface tension and inversely to the radius of the alveoli. Thus, pressure in smaller alveoli would be greater thatn in larger alveoli, if surface tension were the same in both.


Surface tension does not normally cause the collapse of alveoli, however, because pulmonary surfactant (which is a combination of phospholipid and protein secreted by Type II alveolar cells), lowers the surface tension sufficiently by getting between water molecules, reducing their ability to attract each other by hydrogen bonding.


Surfactant prevents surface tension from collapsing the alveoli, which is secreated late in fetal life. Premies are often born with insufficient surfactant this is known as RDS or respiratory distress syndrome- which means the baby has trouble inflating it's lungs. Another example is in the hyaline membrane disease, the lungs of premature infants collapse because of a lack of surfactant. With adults, septic shock can cause acute respiratory distress syndrome or ARDS which decreases compliance and surfactant secretion. This can be do to a respiratory infection causing inflammation in the area.

2. Gas Exchange in the Lungs

To measure atmospheric pressure you can put fluid in a U shaped tube with one end open to the atomosphere and on the other end have it sealed off with a vacuum tube. The atomospheric pressure will then push on the fluid pushing it up towards the sealed off side. Depending on how far it moves, depends on how much atomospheric pressure is in the air, which allows you to measure it. To measure atmospheric pressure, people usually use mercury instead of water because it is more dense. Dalton's law states that whatever gas is in a mixture is going to be equal to the total of the partial pressures. Oxygen itself only takes up about twenty-one percent of our Earths atmosphere.As the altitude increases, the gases start to decrease. After the air has passed through the respiratory zone it is drenched in water vapors. Depending on how warm or cold the temperature depends on how much oxygen its going to hold. In a persons respiratory zone the temperature usually stays at a constant thirty-seven degrees celcius.

With a large area of alveoli and the ability of short diffusion between alveolar air and the capillary blood, allows fast exchange of air and carbon dioxide. When the liquid and gas become at a state of equilibrium the total of gas disolved in the fluid is the one that reaches the maxium value. This value according to Henry's law depends on "the solubility of the gas in the fluid, the temperature of the fluid (more gas can be dissolved in cold water than warm water), and the partial pressure of the gas. The concentration of a gas dissolved in a fluid depends directly on its partial pressure in the gas mixture." Fox, Stuart.


The PO2 in the blood gives us what we need to know of the lung function. The Po2 helps provide valuable information to help people with lung problems such as respiratory stress syndrome. If your Po2 is normal which is about one hundred mmHg, then your red blood cells are almost completely filled with oxygen. You cannot increase the amount of oxygen contained in your lungs by breating in one hundred percent of oxygen, but if you do breath in one hundred percent of oxygen, it will increase the amount of oxygen that is melt into the plasma.Before oxygen can get into the tissue cells it needs to travel from the red blood cells, into the plasma, where it then melts into the tissues. So if the oxygen level increases this process of oxygen diffusion is also going to increase.

In a fetus, the lungs are partially collapsed, so blood is forced through the left atrium to the right atrium through the foramen ovale. After the baby is born the foramen is closed and the vascular resistance of the pulmonary circulation drops steeply. " This fall at birth is due to opening of the vessels as a result of the subatmospheric pressure and physical stretching of the lungs during inspiration and dilation of the pulmonary arterioles in response to increased alveolar Po2." Fox, Stuart. In adults the flow of the pulmonary circulation is equal to that of the systemic circulation.The blood pressure of the pulmonary circulation is lower than that of the systematic capullaries in order to help protect a person against pulmonary edema. This is very serious since it can lead to left ventricular heart failure if there is pulmonary hypertension.

"The total atmospheric pressure increases by one atmosphere (760 mmHg) for every ten m (33 ft) below sea level." Fox, Stuart. If a persons Po2 goes above that of two point five atmospheres, oxygen toxicity may occur. This can happen if a person is breathing in about one hundred percent of air for more than two hours. Effects of oxygen toxicity could lead to a coma or death. If someone gets too much nitrogen in their body, they may have the same symptoms that a drunk might have, such as dizzyness and drowsiness. Decompression sickness can occur if someone is breathing in nitrogen that is causing bubble in the blood. This can lead to the blocking of small blood channels, which can cause serious damage to the person.

3. Regulation of Breathing

Motor neurons that stimulate the respiratory muscles are controlled by two major descending pathways. One controls voluntary breathing and the other controls involuntary breathing. The skeletal muscles, in response to activity in somatic motor neurons in the spinal cord, produce inspiration and expiration.
The respiratory rhythm is generated by a loose aggregation that forms the rhythmicity center for the control of automatic breathing. This center includes different types of neurons that fire at different stages of inspiration. Pons may influence the activity of the medullary rhythmicity center. The apneustic center promotes inspiration by stimulating the neurons in the medulla. The pneumotaxic center antagonizes the apneustic center and inhibits inspiration.

Chemoreceptors are collectively sensitive to changes in the pH of brain interstitial fluid and cerebrospinal fluid. The automatic control of breathing is also influenced by input from chemoreceptors. Central chemoreceptors are in the medulla oblongata. The peripheral chemoreceptors are contained within small nodules associated with the aorta and the carotid arteries. The peripheral chemoreceptors receive blood form critical arteries through small arterial branches.

Chemoreceptor input to the brain stem modifies the rate and depth of breathing so that under normal conditions, arterial PCO2, pH, and PO2 remain relatively constant. Hypoventilation causes PCO2 to rise quickly and pH will fall. Because carbon dioxide can combine with water to form carbonic acid, this causes the pH to fall. During hyperventilation, blood PCO2 will fall quickly and pH rises because of excessive elimination of carbonic acid. Ventilation is adjusted to maintain a constant PCO2. The proper oxygenation of blood occurs naturally as a side product of this reflex control. Hyperventilation causes low CO2 which can result in hypocapnia. Hypoventilation causes high CO2 which can result in hypercapnia.


The lungs contain different types of receptors that influence the brain stem respiratory control centers through sensory fibers in the vagus nerves.
Unmyelinated C fibers are stimulated by noxious substances, such as capsaicin, and can cause apnea followed by rapid, shallow breathing. Irritant receptors are in the wall of the larynx. Rapidly adapting receptors are in the lungs. The irritant receptors can causes a person to cough in response to components of smoke, smog, or inhaled particles. The rapidly adapting receptors are stimulated most directly by an increase in the amount of fluid in the pulmonary interstitial tissue.

The Hering-Breuer reflex is stimulated by pulmonary stretch receptors. During inspiration, the activation of these receptors inhibits the respiratory control centers, making further inspiration more difficult. This reflex is important in newborns to maintain normal ventilation. In adults, the pulmonary stretch receptors are not as active at normal resting tidal volumes, but may contribute to respiratory control at high tidal volumes.

3. Effect of Exercise and High Altitude of Respiratory Function

Changes in ventilation and oxygen delivery occur during exercise and during acclimatization to a high altitude. Neurogenic and humoral mechanisms explain the increased ventilation that occurs during exercise. Neurogenic mechanisms include: sensory nerve activity from the exercising limbs may stimulate the respiratory muscles, or input from the cerebral cortex may stimulate the brain stem centers to modify ventilation. Rapid and deep ventilation continues after exercise has stopped, because the humoral factors in the blood may also stimulate ventilation during exercise. Continued heavy exercise can cause a person to reach lactate threshold. The lactate threshold is the maximum rate of oxygen consumption that can be attained before blood lactic acid levels rise as a result of anaerobic metabolism.


Several adjustments must be made in respiratory function when a person moves significantly higher in elevation. The is necessary to compensate for the decreased PO2 at the higher altitude. Some adjustments can include ventilation, hemoglobin affinity for oxygen, and total hemoglobin concentration. Hypoxic ventilatatory response is when the decreased arterial PO2 stimulates the carotid bodies to produce an increase in ventilation.




Essential Questions:
-How is ventilation accomplished? Incorporate the role of Boyle's Law, as well as the action of muscles, volume change in thoracic cavity during inhalation and exhalation.

Ventilation requires inspiration (inhalation) = breathing in and expiration (exhalation) = breathing out of air. For air to flow into the lungs, intrapulmonary pressure must be lower than atmospheric pressure. This follows from Boyle's Law in which pressure decreases as the volume (of the chest cavity) increases. Therefore, lung expansion is not caused by movement of air into the lungs; it's due to the decrease in pressure that allows air to flow into the lungs. The lungs exhibit both compliance (a measure of the ease at which the lung expands under pressure) and elasticity (the tendency of a structure to return to its initial size after being stretched). To accomplish lung expansion, the diaphragm and external intercostals contract at the onset of inspiration, resulting in the enlargement of the thoracic cavity. The diaphragm descends downward and the external intercostals elevate the ribs and subsequently the sternum upward and outward. Deeper inspirations require more forceful contractions of the diaphragm and external intercostals and the involvement of some neck and thoracic muscles.

Inspiration is always an active process; it requires contraction of inspiratory muscles and energy utilization. During expiration. the diaphragm and external intercostals relax and the lungs recoil due to their elasticity. Intrapulmonary pressure increases and air leaves the lungs out its partial pressure gradient. Expiration is considered a passive process during quiet breathing since it is accomplished by elastic recoil of the lungs on relaxation of the inspiratory muscles, with no muscular exertion or energy expenditure required. Forced expiration (now an active event) requires contraction of the expiratory muscles (the internal intercostals and the abdominal muscles).

How does this apply to PTA:

When working with Patients we as Therapists need to understand how the activities or exercises they are doing effects their breathing. During exercise there is increased ventilation, or hyperpnea, which is matched to the increased metabolic rate so that the arterial blood PCO2 remains normal. This hyperpnea may be caused by proprioceptor information, cerebral input, and/or changes in arterial PCO2 and pH. During heavy exercise the anaerobic threshold may be reached at about 55% of the maximal oxygen uptake. At this point, lactic acid is released into the blood by the muscles. Endurance training enables muscles to utilize oxygen more effectively, so that greater levels of exercise can be performed before the anaerobic threshold is reached.The goal with working with our patients is to improve their strength and endurance and get them back to their best health they can be so that they will be able to do what they want to do or need to do. Example for an athlete who had an injury we will help them strengthen and heal that injury then do endurance training so that when they are healed they can get back to the sport they are doing and hopefully be stronger when they leave then before their injury. Another example is working with a patient who has been sick and stationary for a long time. As a therapist we would build their endurance before strength so that as they move and exercise more the won't be worn out so fast and we can do strengthening training to improve their ADL's and help make their life easier.

3. Fox, Stuart I. "Human Physiology." New York: McGraw-Hill, 2011. Print.