An approximately even distribution of gas (ventilation) and blood (perfusion) in all portions of the lungs
Bronchospasm or mucous plugging, such as in asthma or bronchitis.
That systolic pressure is 120 mmHg above barometric pressure
Breathing.
Millions of molecules moving randomly.
Gas exchange at the cellular level is compromised
To the bases of the lungs, where compliance is greater.
They exert pressure.
The capillary collapses and flow ceases.
At the apex of the lung.
It increases in regular increments.
1. Ventilation of the lungs, 2. Diffusion of oxygen from the alveoli into the capillary blood, 3. Perfusion of systemic capillaries with oxygenated blood, 4. Diffusion of oxygen from systemic capillaries into the cells
The work of breathing.
Because greater pressure causes greater perfusion, and the bases have higher blood pressure.
149 mmHg
From the hila
The pressure or number of collisions.
760 mmHg.
Alveolar pressure is greater than venous pressure but not greater than arterial pressure, allowing blood flow that is somewhat impeded by alveolar pressure.
At the base of the lungs.
Approximately 1000 ml (1 L) of oxygen is transported to the cells each minute.
PaO2 is important because it provides the driving pressure that loads the hemoglobin with oxygen.
The total oxygen content of the blood depends on the amount of oxygen chemically combined with hemoglobin and that dissolved in the blood.
When the abdominal muscles contract, intra-abdominal pressure increases, pushing up the diaphragm and decreasing the volume of the thorax.
An increase in hemoglobin concentration is a major compensatory mechanism in pulmonary diseases that impair gas exchange.
Zero, with pressure varying up or down from zero
Because surface tension increases as the alveoli become larger
Some blood pressure is dissipated in overcoming gravity, resulting in lower blood pressure at the apexes than at the bases.
The portion of the total pressure exerted by any individual gas.
47 mmHg.
Relaxation of respiratory muscles, allowing elastic recoil of the lungs.
No, PaO2 gives little information about the amount of oxygen carried in the blood.
To calculate the total arterial oxygen content, we must know hemoglobin concentration (Hb in grams per deciliter), oxygen saturation (SaO2), and the partial pressure of oxygen (PaO2).
Surface tension refers to the tendency for liquid molecules that are exposed to air to adhere to one another, making expansion of the alveoli difficult.
Normal venous oxygen content is 15 to 16 ml/dl.
Measurement of hemoglobin concentration is important in assessing individuals with pulmonary disease because it helps determine the body's ability to compensate for impaired gas exchange.
Several factors can change the relationship between PaO2 and SaO2.
Alkalosis (high pH) and hypocapnia (decreased PaCO2).
As variations from barometric pressure
An increase in the work of breathing.
It is surrounded by gas-containing alveoli.
Alveolar pressure, gravity, arterial blood pressure, and venous blood pressure.
Arterial and venous pressures are greater than alveolar pressure, and blood flow is not affected by alveolar pressure.
In the bases of the lungs.
It has a large total surface area (70 to 100 m²) and is very thin (0.5 μm).
Inspiration at rest is usually assisted by the diaphragm only.
There are no major muscles of expiration because normal, relaxed expiration is passive and requires no muscular effort.
Oxygen moves from the plasma into the red blood cells (erythrocytes) and binds with hemoglobin molecules.
When the Pa o2 and P ao2 equilibrate, eliminating the pressure gradient across the alveolocapillary membrane.
About 0.3 ml of oxygen.
When hemoglobin molecules bind with oxygen, oxyhemoglobin (HbO2) is formed.
The blood CO2 level is reduced and the affinity of hemoglobin for oxygen is increased.
1. Diffusion of CO2 from the cells into the systemic capillaries, 2. Perfusion of the pulmonary capillary bed by venous blood, 3. Diffusion of CO2 into the alveoli, 4. Removal of CO2 from the lung by ventilation
Spinal deformity or obesity.
In the lower lobes.
By multiplying the percentage of oxygen in the air (20.9%) by the total pressure (760 mmHg), resulting in 159 mmHg.
The outward recoil of the chest wall equals the inward recoil of the lungs.
In the apexes of the lung.
The small amount of oxygen dissolved in plasma is responsible for oxygen’s partial pressure (PaO2) in the blood.
The amount of oxygen in the blood is measured in milliliters per deciliter (1 dl = 100 ml) of blood.
The accessory muscles of expiration are the abdominal and internal intercostal muscles.
To calculate the oxygen content of venous blood, the partial pressure of mixed venous blood (PvO2) and venous oxygen saturation (SvO2) are substituted for the arterial values in the basic formula.
Increases in hemoglobin concentration affect the oxygen content of the blood, while decreases in hemoglobin concentration below the normal value reduce oxygen content.
The body’s initial response to low oxygen content is to accelerate cardiac output.
The binding of hemoglobin with oxygen occurs in the lungs.
Variation from the normal P50.
The temperature and humidity of a gas at the time of measurement
Gravity pulls the lungs down toward the diaphragm and compresses their lower portions or bases
The heart pumps against gravity to perfuse the pulmonary circulation.
Alveolar pressure (gas pressure in the alveoli).
In portions of the lung where blood pressure is lowest and alveolar gas pressure is greatest, such as the apex of the lung.
It becomes saturated with water vapor (humidified) as it passes through the upper airway.
Respiratory muscle contraction.
A small amount dissolves in plasma, and the remainder binds to hemoglobin molecules.
Contraction of external intercostal muscles elevates the anterior portion of the ribs, increasing the volume of the thoracic cavity by increasing its anteroposterior (AP) diameter.
The accessory muscles of inspiration assist when the minute volume is very high, such as during strenuous exercise or when the work of breathing is increased because of disease.
It dissolves in the plasma, where it exerts pressure (the partial pressure of oxygen in arterial blood, or Pa o2).
Surfactant lowers the surface tension by coating the air-liquid interface in the alveoli, making alveolar ventilation or distention possible.
Because oxygen is not very soluble in plasma.
In individuals with both pulmonary and cardiovascular disease, the compensatory mechanism of accelerating cardiac output does not work, making increased hemoglobin concentration an even more important compensatory mechanism.
There would be inadequate saturation of hemoglobin with oxygen.
As variations from barometric pressure
They contain a greater residual volume of gas and are larger and less numerous
A marked increase in oxygen consumption and metabolic demand.
Because more collisions occur in the smaller space.
Three zones.
Above the level of the left atrium.
No, they are not perfectly matched in any of the zones.
Without hemoglobin, oxygen would not reach the cells in amounts sufficient to maintain normal metabolic function.
By using the alveolar gas equation: P AO2 = F iO2 – P aCO2 / 0.8 (the respiratory quotient).
About 0.75 second.
If specific values are known, the oxygen content of arterial blood can be calculated using the hemoglobin concentration, oxygen saturation, and partial pressure of oxygen.
SP-A and SP-D are large hydrophilic molecules called collectins that are capable of inhibiting foreign pathogens.
Arterial pressure (P a) exceeds alveolar pressure, but alveolar pressure exceeds venous pressure (P V). Blood flow occurs in this zone, but alveolar pressure compresses the venules (venous ends of the capillaries).
The affinity of hemoglobin for oxygen decreases.
The arterial portion.
The rapid dissociation of oxygen from hemoglobin.
Increased affinity of hemoglobin for O2.
The areas of the lungs that are most dependent become the best ventilated and perfused when a standing individual assumes a supine or side-lying position.
The pressure exerted by gas molecules in air at specific altitudes.
The temperature of the gas.
Contraction of respiratory muscles, assisted by chest wall recoil.
The normal ˙V/˙Q ratio is 0.8.
The amount of oxygen in the inspired air and the amount of air that remains in the alveoli and tracheobronchial tree between breaths (physiologic dead space).
A pressure gradient of approximately 60 mmHg.
Yes, even during increased cardiac output, which speeds blood flow, shortening the time the blood remains in the capillary.
Until the hemoglobin binding sites are filled or saturated.
Approximately 20 ml of oxygen.
Alveolar pressure (P A) is greater than arterial and venous pressure, and no blood flow occurs.
Hemoglobin’s increased affinity for oxygen, which promotes association in the lungs and inhibits dissociation in the tissues.
Adequate hemoglobin saturation at a variety of altitudes.
The PaO2 at which hemoglobin is 50% saturated, normally 26.6 mmHg.
It increases their speed and the number of collisions.
Oxygen (20.9%), nitrogen (78.1%), and a few other trace gases.
The partial pressure of water vapor (47 mmHg).
Body position has a significant effect on the distribution of pulmonary blood flow.
The diaphragm is a dome-shaped muscle that separates the abdominal and thoracic cavities.
Approximately 104 mmHg.
Only 0.25 second.
The law of Laplace states that the pressure required to inflate a sphere is equal to two times the surface tension divided by the radius of the sphere (P = 2T/r).
Surfactant reverses Laplace’s law by decreasing surface tension as the radius of the alveolus grows smaller and increasing surface tension as the radius grows larger.
Both arterial and venous pressures are greater than alveolar pressure and blood flow fluctuates, depending on the difference between arterial and venous pressures.
The Bohr effect.
Oxygen diffuses rapidly from the blood into tissue cells.
Decreased affinity of hemoglobin for O2.
The decrease in surface tension caused by surfactant.
Alveolar pressure exceeds pulmonary arterial and venous pressures, causing the capillary bed to collapse and normal blood flow to cease.
In the base of the lung.
The partial pressure of oxygen molecules (P o2) is much greater in alveolar gas than in capillary blood.
The maximum amount of oxygen that can be transported by hemoglobin is 1.34 ml/g.
Surfactant is a lipoprotein produced by type II alveolar cells, consisting of 90% lipids and 10% protein, including two groups of surfactant proteins.
Hemoglobin desaturation.
Hemoglobin’s decreased affinity for oxygen or an increase in the ease with which oxyhemoglobin dissociates and oxygen moves into the cells.
Changes in body temperature and levels of 2,3-biphosphoglycerate (2,3-BPG).
Because partial pressure changes of oxygen between 60 and 100 mmHg do not significantly alter the percent saturation of hemoglobin with oxygen.
The elasticity of the lungs is caused by elastin fibers in the alveolar walls and surrounding the small airways and pulmonary capillaries, and by surface tension at the alveolar air-liquid interface.
The relationship between ventilation and perfusion expressed as a ratio called the ventilation-perfusion ratio, or ˙V/˙Q.
When the diaphragm contracts, it flattens downward, increasing the volume of the thoracic cavity and creating a negative pressure that draws gas into the lungs through the upper airways and trachea.
The accessory muscles of inspiration are the sternocleidomastoid and scalene muscles.
The amount of oxygen that can be physically dissolved in blood is 0.003 ml/dl per mmHg.
SP-B and SP-C are small hydrophobic molecules that have a detergent-like effect, separating the liquid molecules and decreasing alveolar surface tension.
If surfactant production is disrupted, alveolar surface tension increases, causing alveolar collapse, decreased lung expansion, increased work of breathing, and severe gas-exchange abnormalities.
The process of hemoglobin binding with oxygen in the lungs is called oxyhemoglobin association or hemoglobin saturation with oxygen.
They shift the curve to the right.
98%.
The surface tension tends to attract fluid into the alveoli.
Surfactant participates in host defense against respiratory pathogens.
The lung and chest wall have elastic properties that permit expansion during inspiration and return to resting volume during expiration.
A distinctive S-shaped curve known as the oxyhemoglobin dissociation curve.
Acidosis (low pH) and hypercapnia (increased PaCO2).
94%, only 4% less than at sea level.
Passive elastic recoil may be insufficient during labored breathing (high minute volume), in which case the accessory muscles of expiration may be needed.
Normal elastic recoil permits passive expiration, eliminating the need for major muscles of expiration.
If disease compromises elastic recoil (e.g., in emphysema) or blocks the conducting airways, the accessory muscles of expiration may be needed.
Normal elastic recoil depends on an equilibrium between opposing forces of recoil in the lungs and chest wall.
The tendency of the chest wall to recoil by expanding is balanced by the tendency of the lungs to recoil or collapse around the hila.
Muscular effort is needed to overcome the resistance of the lungs to expansion.
During expiration, the muscles relax and the elastic recoil of the lungs causes the thorax to decrease in volume until balance between the chest wall and lung recoil forces is reached.
Increased compliance indicates that the lungs or chest wall is abnormally easy to inflate and has lost some elastic recoil.
One half to two thirds of total airway resistance occurs in the nose.
SP-D is postulated to activate macrophages and enhance their recognition of pathogens by increasing their cell surface receptors.
Compliance is the reciprocal of elasticity.
Compliance can be measured with the formula: C = ΔV / ΔP, where C = compliance in liters per centimeter of water, ΔV = volume change (usually tidal volume), and ΔP = pressure change (airway or pleural pressure) in centimeters of water.
Bronchoconstriction, which increases airway resistance, can be caused by stimulation of parasympathetic receptors in the bronchial smooth muscle and by numerous irritants and inflammatory mediators.
Airway resistance increases as the diameter of the airways decreases.
Airway resistance can also be increased by edema of the bronchial mucosa and by airway obstructions such as mucus, tumors, or foreign bodies.
Surfactant is produced from alveolar type II cells and is a complex molecule made up of glycophospholipid, cholesterol, and protein.
The tendency of the lungs to collapse is caused by elastic recoil and surface tension in the alveoli.
If the chest is opened without mechanically ventilating the lungs, the lungs immediately collapse, like inflated balloons that have been released.
During inspiration, the diaphragm and intercostal muscles contract, air flows into the lungs, and the chest wall expands.
Compliance is determined by the alveolar surface tension and the elastic recoil of the lung and chest wall.
The protein component of surfactant includes surfactant proteins A, B, C, and D (SP-A, SP-B, SP-C, SP-D).
SP-A and SP-D regulate the inflammatory response in the lung, have antioxidant properties, and down-regulate allergic reactions.
Elastic recoil is the tendency of the lungs to return to the resting state after inspiration.
When the sternum is split to open the thoracic cavity, the chest wall moves outward laterally.
Bronchodilation, which decreases resistance to airflow, is caused by β2-adrenergic receptor stimulation.
These findings are leading to exciting developments in the synthesis of therapeutic forms of surfactant that may be useful in treating a broad range of pulmonary disorders.
The elasticity of the chest wall is the result of the configuration of its bones and musculature.
Balance between the outward recoil of the chest wall and the inward recoil of the lungs occurs at the resting level, at the end of expiration.
Compliance is the measure of lung and chest wall distensibility, representing the relative ease with which these structures can be stretched.
Compliance is increased in emphysema.
Surfactant prevents infection and acts as an antioxidant both in the alveoli and in extrapulmonary mucosal tissues.
Under normal conditions, the chest wall tends to recoil by expanding outward.
The opposing forces of the chest wall and lungs create, in part, the small negative intrapleural pressure.
Decreased compliance indicates that the lungs or chest wall is abnormally stiff or difficult to inflate.
Compliance is decreased in acute respiratory distress syndrome, pneumonia, pulmonary edema, and fibrosis.
Resistance is computed by dividing change in pressure (P) by rate of flow (F), or R = P/F (Ohm’s law).
The next highest resistance is in the oropharynx and larynx.
There is very little resistance in the conducting airways of the lungs because of their large cross-sectional area.
Surfactant’s primary role is to form a lipid monolayer between the surface of the alveoli and the inspired air, reducing surface tension and preventing expiratory alveolar collapse.
Airway resistance is determined by the length, radius, and cross-sectional area of the airways and by the density, viscosity, and velocity of the gas (Poiseuille’s law).
The work of breathing is determined by the muscular effort (and therefore oxygen and energy) required for ventilation.
SP-A and SP-D are collectins involved in initiating the immune response and clearing pathogens and allergens.
SP-A decreases the growth of certain bacteria and viruses and is also called an opsonin, making microorganisms more vulnerable to phagocytosis.
