The respiratory system is composed of the conducting airways, the respiratory airways, and alveoli (Fig. 12.1).
Conducting and Respiratory Airways
The conducting airways include the nose, mouth, pharynx, larynx, trachea, bronchi, bronchioles, and terminal bronchioles. As their name suggests, these airways merely conduct air to the respiratory airways; they do not participate in gas exchange.
– The bronchi are > 1 mm in diameter and have cartilaginous rings that protect them from collapsing during expiration. They are not embedded in the lung parenchyma, so their diameter is not dependent on lung volume.
– The bronchi branch to form bronchioles that are smaller in diameter and have no supporting cartilage. They are embedded within lung parenchyma, and their diameter expands and contracts with lung volume.
The respiratory airways include the respiratory bronchioles (i.e., bronchioles with alveoli in their walls; Fig. 12.2) and alveolar ducts.
Alveoli. There are ~300 million alveoli in adult lungs, each being ~250μm in diameter. Their walls are composed of a simple squamous epithelium, primarily type I pneumocytes. Each alveolus is encased by pulmonary capillaries, which are sandwiched between the lumens of adjacent alveoli. The total surface area available for gas exchange is ~150 m2.
Clinical implications of the anatomy of the bronchi
Improperly placed endotracheal (ET) tubes or aspirated foreign bodies are more likely to become lodged in the right main bronchus than the left. This is because the left bronchus diverges sharply at the tracheal bifurcation, whereas the right bronchus is relatively straight.
Drug delivery via endotracheal tubes
Endotracheal (ET) tubes are used to maintain airway patency and facilitate ventilation in an emergency situation. When intravenous (IV) access cannot be obtained, drugs (e.g., epinephrine, nalaxone, atropine, and lido-caine) are sometimes given via ET tubes. They can exert local or systemic effects.
Pressures in the Lungs
To understand the mechanics of ventilation and airflow during breathing, it is necessary to review the pressure in the lungs.
– Intrapleural pressure is the pressure that is generated between the lungs and chest wall by the opposing forces created by the elastic recoil of the lungs and the elastic recoil of the chest wall.
– Alveolar pressure is the pressure within the alveoli.
– Transpulmonary pressure is alveolar pressure minus intrapleural pressure.
Intrapleural pressure is always less than alveolar pressure; therefore, transpulmonary pressure is always positive. It is the positive transpulmonary pressure that keeps the lungs inflated (like a balloon) against the chest wall.
Fig. 12.1 Conducting and respiratory parts of the bronchial tree.
The bronchial tree branches into successively finer divisions. The bronchi are reinforced by cartilage rings or plates and are lined by pseudostratified columnar, ciliated epithelium that contains goblet cells. The bronchioles do not have cartilage.
From Thieme Atlas of Anatomy, Neck and Internal Organs, © Thieme 2006, Illustration by Markus Voll.
Fig. 12.2 Structure of a respiratory bronchiole.
Alveoli first begin to appear on the respiratory bronchioles, marking the start of the respiratory portion of the lung. These alveoli are isolated initially, then become more numerous and are collected into sacs. Each sac has a central open space, or alveolar duct, that is continuous with the lumen of its respiratory bronchiole. The alveolar walls are composed of squamous epithelium and are in direct contact with the pulmonary capillaries for gas exchange to occur. Connective tissue with abundant elastic fibers is found throughout the branches of the bronchial tree and the alveoli. These contribute substantially to the elastic recoil of the lungs during expiration.
From Thieme Atlas of Anatomy, Neck and Internal Organs, © Thieme 2006, Illustration by Markus Voll.
Ventilation (breathing) is the process by which air enters and exits the lungs. Respiration is the overall term for ventilation, gas exchange, and utilization in cells.
Mechanics of Ventilation
Ventilation occurs in a cyclical manner with alternating inspiratory and expiratory phases.
Inspiration is an active process and is principally mediated by the diaphragm during quiet breathing.
– Contraction of the diaphragm enlarges the chest cavity, reducing intrapleural pressure. This increases the transpulmonary pressure and expands the lungs (Fig. 12.3). Minimal movement of the diaphragm (a few centimeters) is sufficient to move several liters of gas.
– The external intercostal and accessory muscles are not necessary for resting respiration, but they contribute substantially to deep respiration during exercise and respiratory distress.
Expiration is a passive process during quiet breathing. When the diaphragm relaxes, air is expelled from the lungs due to the elastic recoil of the lung–chest wall system. Active expiration (using muscles of expiration) occurs during exercise or in obstructive lung disease.
Fig. 12.3 Mechanics of ventilation.
When the diaphragm moves to the inspiratory position (red), the ribs are elevated by the intercostal muscles (chiefly the external intercostals) and scalene muscles. Because the ribs are curved and directed obliquely downward, elevation of the ribs expands the chest transversely (toward the flanks) and anteriorly. Meanwhile, the diaphragm leaflets are lowered by muscle contraction causing the chest to expand inferiorly. These processes result in overall expansion of the thoracic volume. When the diaphragm moves to the expiratory position (blue), the chest becomes smaller in all dimensions, and the thoracic volume is decreased. This process does not require additional muscular energy. The muscles that are active during inspiration are relaxed, and the lung contracts as the elastic fibers in the lung tissue that were stretched on inspiration release their stored energy, causing elastic recoil. For forcible expiration, however, the muscles that assist expiration (mainly the internal intercostal muscles) can actively lower the rib cage more rapidly and to a greater extent than is possible by passive recoil alone.
From Thieme Atlas of Anatomy, Neck and Internal Organs, © Thieme 2006, Illustration by Markus Voll.
– The rectus abdominus, external and internal obliques, and transverse abdominals contribute to active expiration by forcing abdominal contents upward against the diaphragm. This causes an increase in intrapleural pressure, which compresses the alveoli, allowing the expulsion of air.
– The internal intercostal muscles stiffen the chest during expiration, preventing bulging of the chest and minimizing changes in chest volume.
Compliance of the Respiratory System
Lung compliance expresses the distensibility of the lungs, that is, how easily the lungs expand when transpulmonary pressure increases. It is expressed by the following equation:
C = ΔV/ΔP
C = lung compliance
ΔV = increase in lung volume (mL)
ΔP = increase in transpulmonary pressure (mm Hg).
– Compliance is inversely related to stiffness.
– Compliance is inversely related to the elastic recoil, or elastance, of the lung. Recoil causes the lungs to return to their previous volume when stretching ceases following an increase in transpulmonary pressure. It is mediated by surface tension in the alveoli and by elastic fibers in the lung connective tissue.
Compliance of the Lung–Chest Wall Combination
Because the lungs and chest wall expand and contract together, the overall compliance of the respiratory system is that of the lung–chest wall combination. The compliance of the lung–chest wall combination is lower than the compliance of the lungs alone or chest wall alone.
– The compliance of the lung–chest wall combination varies with lung volume. Compliance is highest at the normal resting volume (functional residual capacity [FRC]) and decreases at both very low and very high volumes.
– At low volumes, compression of the chest wall reduces compliance.
– At high volumes, the increased stretch of elastic tissues in the lung parenchyma causes the lungs to get stiffer (less compliant). High transpulmonary pressure is required to drive this increase in volume, but it is not responsible for the decrease in compliance.
Changes in Lung Compliance in Disease States
– Lung compliance is decreased in pulmonary fibrosis because the interstitium surrounding the alveoli becomes infiltrated with inelastic collagen.
– Lung compliance is increased in emphysema because many small alveoli are replaced by fewer but larger coalesced air spaces that have less elastic recoil.
Pulmonary fibrosis is a restrictive lung disease in which repeated lung injury leads to the inflammation of alveoli and interstitium and eventual scarring. In restrictive lung disease, the ability of the lungs to expand is reduced (↓ compliance of the lung–chest wall). There is also an impairment of diffusion due to a decrease in diffusion surface area and an increase in diffusion distance. Pulmonary fibrosis may be idiopathic, or it can be caused by several factors, including connective tissue disease (e.g., rheumatoid arthritis and systemic lupus erythematosus), drugs (e.g., bleomycin and amiodarone), hepatitis, ulcerative colitis, radiation, and environmental pollutants. Symptoms include exertional shortness of breath (dyspnea), dry cough, fatigue, weight loss, and joint pain (arthralgia). Complications are hypoxemia (low oxygen content of blood), pulmonary hypertension, and right-sided heart failure secondary to pulmonary hypertension (cor pulmonale). Respiratory failure may occur at the end stage. Lung function tests reflect decreased lung volumes and gas exchange. Treatment involves the use of immunosuppressant drugs (e.g., prednisone and methotrexate). Lung transplantation may be considered in younger patients when fibrosis is severe.
Surface Tension in the Alveoli
Surface tension is due to the cohesive forces between water molecules at the air–water interface in the alveoli of lungs. It acts to contract the alveoli and is a major contributor to the force of elastic recoil of the lung.
If there were no opposing force, surface tension would cause the alveoli to collapse (atelectasis). However, the collapsing force is opposed by transpulmonary pressure, which is always positive, allowing the alveoli to remain open.
According to the law of Laplace, the transpulmonary pressure P (in dynes/cm2) required to prevent collapse of an alveolus is directly proportional to surface tension T (in dynes/cm), and inversely proportional to alveolar radius r (in cm), as expressed by
P = 2T/r
– All alveoli in a given region of the lungs have about the same transpulmonary pressure. If they all had the same surface tension, the Laplace relationship predicts that the smaller alveoli would collapse and force their volume into larger alveoli. However, surface tension is reduced by pulmonary surfactant, and the reduction is greater in small alveoli than in larger ones because small alveoli concentrate the surfactant. Thus, the increased tendency to collapse because of small radius is just balanced by a greater reduction in surface tension.
Surfactant is a complex substance, consisting of proteins and phospholipids (mainly dipalmitoyl lecithin), that is produced in type II pneumocytes. It lines alveoli and lowers surface tension by the same mechanism as detergents and soaps (i.e., it coats the water surface and reduces cohesive interactions between water molecules).
As an extension of its role in lowering surface tension, surfactant also produces the following effects:
– It increases compliance at all lung volumes, which allows for easier lung inflation and greatl y decreases the work of breathing.
– It reduces the otherwise highly negative pressure in the interstitial space, which reduces the rate of filtration from pulmonary capillaries. This assists in maintaining lungs without excessive water.
Failure of surfactant production and/or excessive surfactant breakdown occurs in neonatal respiratory distress syndrome (RDS).
Neonatal respiratory distress syndrome
Neonatal RDS is a hyaline membrane disease that is caused when a deficiency in surfactant leads to alveolar collapse (atelectasis). It normally occurs in babies born before 28 weeks. Symptoms usually start within minutes of birth and may include absence of breathing (apnea), shortness of breath (dyspnea), increased rate of breathing (tachypnea), grunting, nasal flaring, chest wall retractions, and cyanosis. Complications include pneumothorax (air in the pleural space) and intracranial hemorrhage. Treatment involves the use of continuous positive airway pressure (CPAP) to help maintain airway patency and the administration of beractant (a natural bovine-derived surfactant) or colfosceril (a synthetic surfactant). These agents are given by tracheal instillation. Neonatal RDS may be prevented by the administration of corticosteroids to the mother 24 hours prior to delivery of a premature baby to hasten surfactant production.
Test for fetal lung maturity
Fetal lung maturity can be tested by extracting a sample of amniotic fluid and measuring the lecithin:sphingomyelin ratio (S/L ratio). An S/L ratio < 2:1 indicates surfactant deficiency and therefore lung immaturity.
Pneumothorax occurs when air is admitted into the pleural space between the lung and the chest wall. This causes an increase in intrapleural pressure and a decrease in trans-pulmonary pressure, which may lead to partial or complete lung collapse. A primary pneumothorax can occur spontaneously due to rupture of a pleural bleb. Pneumothoraces may also occur secondarily to lung disease, for example, chronic obstructive pulmonary disease (COPD), asthma, tuberculosis (TB), pneumonia, cystic fibrosis, and lung cancer. They may also occur due to penetrating chest trauma. Symptoms include shortness of breath (dyspnea), the severity of which depends on the degree of lung collapse; sudden, sharp chest pain that is exacerbated by taking a deep breath or coughing; chest tightness; and increased heart rate (tachycardia). Signs may be subtle but include diminished breath sounds and chest expansion on the affected side and hyper-resonance to percussion. No treatment may be required for small pneumothoraces that heal spontaneously. Larger pneumothoraces require placement of a chest tube or surgical repair (rarely).
Tension pneumothorax is a life-threatening condition in which air accumulates in the pleural space and becomes trapped when the injured tissue acts as a one-way valve. This causes complete collapse of the lung on the affected side and the heart to shift to the opposite side, thus compromising venous return and cardiac output. The ventilatory capacity of the other lung is also impaired due to compression. Signs include respiratory distress, increased heart rate (tachycardia), distended neck veins, hypotension, and tracheal deviation (away from the side of tension pneumothorax). Complications include hypoxemia (low blood oxygen), respiratory failure, shock, and cardiac arrest. Treatment for this condition is emergency needle decompression of the affected side (the side opposite that to which the trachea is deviated) followed by placement of a chest tube.
Airflow through the Bronchial Tree
Airflow through the bronchial tree obeys the same principles as blood flow through blood vessels except that the viscosity of air is much lower than that of blood. Airflow is related to the driving pressure and the resistance to flow by
Q = ΔP/R
where Q is airflow (mL/min), ΔP is pressure gradient between the mouth/nose and alveoli (cm H2O), and R is airway resistance (cm H2O/mL/min).
– Airflow is directly proportional to the pressure difference between the mouth/nose and the alveoli and inversely proportional to airway resistance.
Resistance is derived from Poiseuille’s equation as expressed by
R = 8ηL/πr4
where R is airway resistance, r is radius of the airway (cm), η is viscosity of air, and L is length of the airway.
– Like the circulatory system, the length of the bronchial tree is relatively constant, as is the viscosity of inspired air. Therefore, any changes in resistance to airflow are mainly due to changes in the radius of the airways. Because resistance is inversely proportional to the airway radius to the fourth power, small changes in diameter cause large changes in resistance.
– The large airways offer little resistance to airflow. The small airways individually have high resistance, but their enormous number in parallel reduces their combined resistance to a small value. Therefore, the sites of highest resistance in the bronchial tree are normally in the medium airways.
Chronic obstructive pulmonary disease
COPD is a term used to describe chronic obstructive bronchitis and emphysema, which always coexist, to varying degrees. With chronic bronchitis, inflammation (most commonly caused by cigarette smoke) causes the bronchial tubes to thicken and scar and produce excess mucus. This causes narrowing of the airway lumen and obstruction. Emphysema occurs when the walls of the alveoli are progressively destroyed. This decreases the surface area of the alveoli for gas exchange with pulmonary capillary blood and causes the small airways to collapse during expiration, trapping air in the lungs. This may be caused by cigarette smoke or α1-antitrypsin deficiency. The characteristic symptoms of COPD are persistent cough, sputum, dyspnea, and wheeze. Signs of COPD include hyperinflation of the lungs, causing a barrel chest appearance, hypertrophy of accessory muscles of respiration, descended trachea, respiratory distress, crepitations, and wheeze. Lung function tests show that the forced expiratory volume/forced vital capacity is < 70%, and residual volume and total lung capacity are high. Drugs used to treat COPD include bronchodilators (β2-agonist drugs), inhaled corticosteroids, and antibiotics (when necessary).
Pink puffers and blue bloaters
Some patients with COPD increase their respiratory rate (hyperventilate) to try to cope with their shortness of breath (dyspnea). In this way, they manage to achieve relatively normal oxygenation of arterial blood, and their blood CO2 concentration can be either normal or low. They are termed “pink puffers” because they are breathless and pink from the exertion. Other patients with COPD do not have the muscle or lung capacity to increase their respiratory rate. They have low oxygenation of arterial blood and high blood CO2 concentrations, and so appear blue. Right-sided heart failure may develop secondary to pulmonary hypertension (cor pulmonale), resulting in edema and “bloating.”
Regulation of Airway Resistance. Airway resistance is primarily regulated by modulation of airway radius by the parasympathetic and sympathetic nervous systems.
– Parasympathetic nervous system: Vagal stimulation releases acetylcholine that acts on muscarinic (M3) receptors in the lungs, leading to bronchoconstriction. This increases the resistance to airflow.
– Sympathetic nervous system: Postganglionic sympathetic nerves release norepinephrine that act on β2 receptors, leading to bronchodilation. This decreases the resistance to airflow.
Asthma is predominantly an inflammatory disease with associated bronchospasm (sudden constriction of the smooth muscle in the walls of the bronchioles), mucosal swelling, and increased mucus production. There is episodic bronchial obstruction causing wheezing, shortness of breath (dyspnea), cough, and mucosal edema. The inflammatory response may be triggered by allergens such as animal hair, dust mites, feathers, pollen, and mold. In nonallergic asthma, bronchial hyperreactivity may be caused by the inhalation of chemicals, cigarette smoke, viral infections, cold air, exercise, and stress. Drugs (e.g., aspirin and or other nonsteroidal antiinflammatory drugs [NSAIDS]) can also precipitate bronchospasm. This can be serious and sometimes fatal; therefore, these drugs are contraindicated in patients with asthma who have a history of hypersensitivity reactions and should be used with caution in all asthmatics. Acetaminophen can be used by asthmatics to treat mild to moderate pain.
Relationship of Pressures and Airflow during the Breathing Cycle
– Prior to inspiration, pressures within the airways and alveoli are zero (i.e., equal to external barometric pressure), and intrapleural pressure is about –5 mm Hg, yielding a transpulmonary pressure of +5 mm Hg. This positive pressure just balances the elastic recoil of the lung–chest wall combination. There is no airflow.
– During inspiration, the thoracic cavity expands, making intrapleural pressure more negative by several mm Hg and making transpulmonary pressure more positive by the same amount (Fig. 12.4). The increase in transpulmonary pressure causes expansion of the lungs. The increasing volume of the lungs lowers alveolar pressure by ~1 mm Hg, thereby creating a positive driving pressure between the trachea and alveolar space. This causes air to flow through the bronchial tree into the alveoli.
– During expiration, the diaphragm relaxes. The lung–chest wall, now expanded at the end of inspiration, has greater elastic recoil than at rest and contracts. The compression of the lungs increases alveolar pressure by ~1 mm Hg, driving air out of the lungs through the trachea. As the lungs get smaller during exhalation, their elastic recoil diminishes, trans-pulmonary pressure falls, and intrapleural pressure rises (becomes less negative) back to its resting value.
Fig. 12.4 Alveolar pressure (PA) and intrapleural pressure (Ppl) during respiration.
During inspiration, intrapleural pressure becomes more negative, and the transpulmonary pressure (PTP) becomes more positive. This causes alveolar pressure (PA) to fall. During expiration, PA increases, PTP falls, and Ppl rises back to its original value. Vpulm, respiratory volume.
Fig. 12.5 Lung volumes and capacities. FRC, functional residual capacity.
Lung Volumes and Capacities
– Lung volumes are a way to functionally divide volumes of air that occur during different phases of the breathing cycle (Fig. 12.5). They are all measured by spirometry, except for residual volume. They vary with height, sex, and age.
– Lung capacities are the sums of two or more lung volumes.
– Tidal, inspiratory, and expiratory reserve volumes and inspirational and vital capacities are used in basic pulmonary function tests.
– Tidal volume (TV) is the volume of air that moves in or out of the lungs during one normal, resting inspiration or expiration.
– Inspiratory reserve volume (IRV) is the volume of air that can be inspired beyond a normal inspiration.
– Expiratory reserve volume (ERV) is the volume of air that can be expired beyond a normal expiration.
– Residual volume (RV) is the volume of air left in the lungs and airways after maximal expiration.
Table 12.1 contains the normal approximate lung volumes and expresses them as a percentage of total lung capacity (TLC).
– Inspirational capacity (IC) is the maximum volume of air that can be inspired with a deep breath following a normal expiration. It is the sum of TV and IRV.
– Functional residual capacity (FRC) is the volume of the lungs after passive expiration with relaxed respiratory muscles. It is the sum of ERV and RV.
– Vital capacity (VC), or forced vital capacity (FVC), is the maximum volume of air that can be expired in one breath after deep inspiration. It is the sum of TV, IRV, and ERV.
– TLC is the total volume of air that can be contained in the lungs and airways after a deep inspiration. It is the sum of all four lung volumes: TV, IRV, ERV, and RV.
Note: TLC and FRC cannot be measured by spirometry because residual volume is needed for their calculation.
Table 12.2 contains the normal lung capacity volumes.
Forced Expiratory Volume
FEV1 is the volume of air that can be forcibly expired in the first second following a deep breath (Fig. 12.6). It is usually > 70% of the FVC (FEV1/FVC > 70%).
– In obstructive lung disease (e.g., asthma and COPD), FEV1 is reduced proportionally more than FVC; therefore, FEV1/FVC < 70%.
– In restrictive lung disease (e.g., fibrosis), both FEV1 and FVC are reduced. This means that FEV1/FVC is normal or increased.
Dead space is volume within the bronchial tree that is ventilated but does not participate in gas exchange.
– Anatomical dead space is the volume of the conducting airways (pharynx, trachea, and bronchi) that do not contain alveoli and therefore cannot participate in gas exchange. It is ~150 to 200 mL.
– Physiological dead space is the total volume of the bronchial tree that is ventilated but does not participate in gas exchange.
Fig. 12.6 Volume exhaled versus time during a forced exhalation.
The total volume exhaled is the forced vital capacity (FVC), and the volume exhaled in the first second is the forced expiratory volume (FEV1).
– In healthy lungs, physiological dead space is approximately equal to anatomical dead space. However, physiological dead space may be increased in lung diseases where there are mismatches between ventilation (V) and perfusion (pulmonary blood flow [Q]).
– Physiological dead space can be calculated using Bohr’s equation. This calculation assumes that the partial pressure of CO2 (Paco2) in the alveoli is the same as that in systemic arterial blood.
VD/VT = (Paco2 − Peco2)/Paco2
where VD is physiological dead space (mL), VT is tidal volume (mL), PaCO2 is arterial PCO2 (mm Hg), and PECO2 is mixed expired PCO2 (mm Hg).
– This equation, which expresses physiological dead space as a fraction of the exhaled TV, accounts for the fact that mixed expired PCO2 is lower than alveolar PCO2 due to the dilution of alveolar PCO2 with dead space air (containing no CO2).
Example: PaCO2 = 41 mm Hg; PECO2 = 28.7 mm Hg
VD/VT = (41 − 28.7)/41 = 0.3
So, dead space is 30% of tidal volume, or VD = 150 mL when VT = 500 mL.
Minute ventilation refers to the total ventilation per minute. It is expressed as
Minute ventilation = TV × breaths/min
Alveolar ventilation refers to ventilation of alveoli that participate in gas exchange per minute. It is expressed as
Alveolar ventilation = (TV – physiological dead space) × breaths/min
12.2 Pulmonary Blood Flow
The pulmonary circulation is discussed in Chapter 10.
Distribution of Pulmonary Blood Flow
When a person is upright, the force of gravity affects the distribution of pulmonary blood flow within the lungs (but not the total amount of blood flow) because vascular pressures progressively fall at locations above the heart. This distribution of blood flow is described in terms of “zones” of the lung.
Zone 1: Lung Apex. If pulmonary artery pressure is not high enough to support the column of blood from the right ventricle all the way to the apices of the lungs, the uppermost blood vessels collapse, and there is no flow in this region. This does not normally occur in healthy lungs but may occur if right ventricular pressure is extremely low (e.g., due to hemorrhage). Also, if alveolar pressure is increased to the point where it exceeds vascular pressure, blood vessels collapse (e.g., due to positive pressure ventilation).
Zone 2: Middle of the Lung. In zone 2, blood flow is intermittent. Pulmonary artery pressure drives blood flow at its peak during systole, but not during the rest of the cardiac cycle.
Zone 3: Lung Base. Zone 3 has no gravitational impediment to blood flow because regions located below the heart always have vascular pressures greater than alveolar pressure. Therefore, blood flow is continuous.
– Right-to-left shunts allow blood to move directly from the pulmonary circulation to the systemic circulation.
– Intracardiac right-to-left shunts occur in cases where right ventricular pressure is greater than left ventricular pressure due to right ventricular hypertrophy (increased size of the muscle of the right ventricle).
– Right-to-left shunts can also occur through regions of the lung that are perfused but not ventilated due to infection (e.g., pneumonia) or injury (e.g., chemical inhalation).
– The result of a right-to-left shunt is decreased oxygenation of the blood (hypoxemia).
– Left-to-right shunts allow blood to recirculate from the systemic circulation back to the pulmonary circulation.
– Left-to-right shunts usually occur through atrial or ventricular septal defects and result in the right ventricle pumping more blood than the left ventricle. This increases the work of the right ventricle and may lead to right ventricular hypertrophy.
– There is no hypoxemia.
Capillary Exchange of Fluid in the Lungs
Fluid outside the alveoli in the interstitial space is governed by Starling forces as it is in all other capillary beds (see Chapter 10). Although pulmonary capillary hydrostatic pressure (Pc) is normally low, the negative interstitial hydrostatic pressure (Pi) and the finite interstitial fluid oncotic pressure (πi) favor net filtration of fluid out of pulmonary capillaries into the interstitium at a modest rate. The filtered fluid is removed via the pulmonary lymphatic system. If the rate of filtration exceeds the capacity of the lymphatic system to remove it, the result is pulmonary edema.
Pulmonary edema is the accumulation of fluid in the lungs. It begins as fluid in the interstitial spaces and if severe enough, spreads to the alveoli. There are two types: cardiogenic and noncardiogenic. The cardiogenic type occurs in heart failure when left atrial pressure, and hence pulmonary venous pressure, rises too high. The noncardiogenic type occurs in lung disease or injury that allows protein to leak from the capillaries, thereby raising the oncotic pressure in the interstitium. The main consequences of pulmonary edema are reduced lung compliance, which increases the work of breathing, and poor oxygenation due to a ventilation/perfusion mismatch. Signs and symptoms begin with shortness of breath (dyspnea), rapid breathing (tachypnea), anxiety, and hypoxemia (low blood oxygen). The patient may cough up blood (hemoptysis) and produce pink, frothy sputum. Treatment is directed at the underlying cause, and supplemental oxygen is administered.