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Flashcards in Respiratory Deck (163)

Conducting zone in the respiratory tree

The large airways consist of nose, pharynx, larynx, trachea, and bronchi. Small airways consist of bronchioles that further divide into terminal bronchioles (a large number of parallel creates the least resistance. They are responsible for warms, humidifies, and filters air but does not participate in gas exchange (anatomic dead space). Cartilage and goblet cells extend to the end of the bronchi. Pseudostratified ciliated columnar cells (clear mucus from lungs) extend to beginning of terminal bronchioles, then transition to cuboidal cells. Airway smooth muscle cells extend to the end of terminal bronchioles.


Respiratory zone

It is located in the lung parenchyma and consists of respiratory bronchioles, alveolar ducts, and alveoli. It participates in gas exchange. There are mostly cuboidal cells in respiratory bronchioles, then simple squamous cells up to the alveoli. Cilia terminate in the respiratory bronchioles. Alveolar macrophages clear debris and participate in immune responses.


Type I pneumocytes

They cover 97% of alveolar surfaces and line the alveoli. They are squamous; Thin is optimal for gas diffusion.


Type II pneumocytes

They secrete pulmonary surfactant, which decreases alveolar surface tension and prevents alveolar collapse (atelectasis). They are cuboidal and clustered. They also serve as precursors to type I cells and other type II cells. Type II cells proliferate during lung damage.


Club (Clara) cells

They are nonciliated, low columnar/cuboidal with secretory granules. They secrete a component of surfactant, degrade toxins, and act as a reserve cell.


Collapsing pressure (P)

P=(2 x surface tension)/radius. Alveoli have an increased tendency to collapse on expiration as radius increases (law of Laplace).



Pulmonary surfactant is a complex mix of lecithins, the most important of which is dipalmitoylphosphatidylcholine. Surfactant synthesis begins around week 26 of gestation, but mature levels are not achieved until around week 35. Lecithin to sphingomyelin ration is over 2 in amniotic fluid indicates fetal lung maturity.


Lung anatomy

The right lung has three lobes; Left has Less Lobes (2) and Lingula (homolog of the right middle lobe). The right lung is more common site for inhaled foreign body because the right main stem bronchus is wider and more vertical than the left. If you aspirate a peanut: while upright, it enters the lower portion of the right inferior lobe; while supine, it enters superior portion of the right inferior lobe. Instead of a middle lobe, the left lung has a space occupied by the heart. The relationship of the pulmonary artery to the bronchus at each lung hilum is described by RALS: Right Anterior, Left Superior.


Structures perforating the diaphragm

At T8, IVC passes through. At T10, esophagus and vagus (CN 10; 2 trunks) passes through. At T12, aorta (red), thoracic duct (white), azygos vein (blue) passes through (At T-1-2 its the red, white and blue). I (IVC) ate (8) ten (10) eggs (esophagus) at (aorta) twelve (12).


Innervation of the diaphragm

It is innervated by C3, 4, and 5 (phrenic nerve), which keeps the diaphragm alive. Pain from the diaphragm irritation (eg air or blood in the peritonial cavity) can be referred to shoulder (C5) and trapezius ridge (C3, C4).


Level of the common carotid bifurcation

Bifourcates at C4.


Level of the trachea bifurcation

Bifourcates at T4.


Level of the abdominal aorta bifurcation

Bifourcates at L4.


Inspiratory reserve volume (IRV)

Air that can still be breathed in after a normal inspiration.


Tidal volume (TV)

Air that moves into the lung with each quiet inspiration, typically around 500mL.


Expiratory reserve volume (ERV)

Air than can still be breathed out after a normal expiration.


Residual volume (RV)

The air in lung after maximal expiration. It cannot be measured on spirometry.


Inspiratory capacity (IC)

Inspiratory reserve volume (IRV) + tidal volume (TV)


Functional residual capacity (FRC

Expiratory reserve volume (ERV) + residual volume (RV). It is the volume of gas in lungs after normal expiration.


Vital capacity (VC)

Inspiratory reserve volume (IRV) + tidal volume (TV) + expiratory reserve volume (ERV). It is the maximum volume of gas that can be expired after a maxima inspiration.


Total lung capacity (TLC)

Inspiratory reserve volume (IRV) + tidal volume (TV) + expiratory reserve volume (ERV) + residual volume (RV). It is volume of gas present in lungs after a maximal inspiration.


Determination of physiologic dead space

Vd=physiologic dead space= anatomic dead space of conducting airways plus alveolar dead space. The apex of a healthy lung is the largest contributor of alveolar dead space. Volume of inspired air that does not take part in gas exchange. Vd = Vt x (PaCO2 -PeCO2)/PaCO2. Vt = tidal volume. PaCO2= arterial PCO2. PeCO2 = expired air PCO2. (Taco, Paco, PEco, Paco is the order of variables in the equation).


Minute ventilation (Ve)

Total volume of gas entering lungs per minute. Ve= Vt x respiratory rate (RR). Vt = tidal volume.


Alveolar ventilation (Va)

Volume of gas per unit of time that reaches the alveoli. Va=(Vt-Vd) x RR.


Elasticity of the lung and chest wall

Elastic recoil is the tendency for lungs to collapse inward and chest wall to spring outward. At functional residual capacity, the inward pull of the lung is balanced by the outward pull of the chest wall, and system pressure is atmospheric. Elastic properties of both the chest wall and lungs determine their combined volume. At functional residual capacity, airway and alveolar pressures are 0, and intrapleural pressure is negative (which prevents a pneumothorax). Pulmonary vascular resistance is at a minimum.


Compliance of the lung and chest wall

Is the change in lung volume for a given change in pressure. It decreases in pulmonary fibrosis, pneumonia, pulmonary edema. It increases in emphysema and normal aging.



Hemoglobin is a tetramer (consisting of 4 subunits), with each subunit containing a centric heme molecule. Each heme molecule can carry 1 oxygen molecule. Hemoglobin has several variants including: Hemoglobin A (α2β2) which is found in adults; Hemoglobin A2 (α2δ2), which is also found in adults but in lesser quantities; Hemoglobin F (α2γ2), found predominately in fetal life.


Taut vs relaxed hemoglobin

Hemoglobin's subunits switch between two conformations with different affinities for oxygen: The Taut (T) form has a low affinity for oxygen and the Relaxed (R) form has a high affinity for oxygen (over 300x). When two oxygen molecules are bound to hemoglobin in the taut conformation, its conformation switches to the relaxed form so that all four heme sites may be filled, occurring in a high oxygen tension environment (e.g. lungs). The relaxed conformation of hemoglobin switches to the taut conformation under times of low oxygen tension, such as in the peripheral tissues where oxygen needs to be unloaded. Hemoglobin acts a buffer for H ions. Hemoglobin modifications (eg methemoglobin and carboxyhemoglobin) lead to tissue hypoxia from decreased O2 saturation and decreased O2 content.


Specific conditions favor the taut hemoglobin conformation over the relaxed conformation

Specific conditions favor the taut hemoglobin conformation over the relaxed conformation, allowing oxygen to be unloaded peripherally and moving the oxygen dissociation curve to the right: CO2 allosterically binding the N-terminus; Acidic environments (i.e. low pH); 2,3-DPG (Fetal Hb has a lower affinity than adult Hb and thus has a higher affinity for O2), produced during glycolysis and stabilizes the taut conformation; Elevation by decreasing oxygen tension; Temperature elevation. Mnemonic: A CADET faces right.



Carboxyhemoglobin, resulting from carbon monoxide poisoning or chronic tobacco smoking, produces a cherry-red appearance of the skin typically in deceased patients. Treatment for carboxyhemoglobinemia is 100% O2 or hyperbaric O2.



Methemoglobinemia results from oxidation of ferrous iron (Fe2+) to ferric iron (Fe3+) leading to a reduced affinity for oxygen. Classic findings for patients with methemoglobinemia include cyanosis and chocolate colored blood. The most common chemicals and drugs that may cause acquired methemoglobinemia: Anesthetics (e.g. benzocaine), Benzenes, Antibiotics (e.g. dapsone, chloroquine, sulfonamides), Nitrites (used as additives to prevent meat from spoiling). Methemoglobinemia is treated with: Methylene blue, acting as a cofactor to propagate the methemoglobin to hemoglobin transition; Vitamin C, which may be beneficial by acting as an electron donor to limit reactive oxygen species formation or by altering iron levels



Myoglobin is similar in structure to hemoglobin, but is a monomer.


Oxygen-hemoglobin dissociation curve

The oxygen-hemoglobin dissociation curve is a plot of percent saturation of hemoglobin as a function of pO2. The curve has a sigmoidal shape, which reflects the positive cooperativity of hemoglobin. Positive cooperativity of hemoglobin refers to the fact that when each O2 binds hemoglobin, the resulting conformational change in the hemoglobin molecule causes an increase in its affinity for additional O2 molecules (until fully saturated). The p50 of a curve (pO2 at which 50% saturation is achieved) can be used to compare different curves with one another. The normal value for p50 is 26.7mmHg.


Right shift of the hemoglobin dissociation curve

When P50 is greater than 26.7mmHg, the hemoglobin dissociation curve is said to exhibit a "right shift." With a right shift, hemoglobin has less affinity for O2, which facilitates unloading of O2 in the tissues. Right shift occurs with: Increased temperature (ex: tissues with increased metabolic activity); Increased [H+] (decreased pH); Higher altitude; Increased [2,3-BPG] (aka 2,3-DPG); CHRONIC anemia, which causes an increase in [2,3-BPG]. The factors that cause a right shift in the oxygen hemoglobin dissociation curve can be remembered with mnemonic (CADETs face right): CO2 (increased [CO2] ); Acidosis, Anemia; 2,3-DPG; Elevation; Temperature increase.


Left shift of the hemoglobin dissociation curve

A "left shift" of the oxygen hemoglobin dissociation curve refers to when the p50


Oxygen content of blood

O2 content = (O2 binding capacity x % saturation) + dissolved O2. Normally 1 g Hb can bind 1.34 mL O2. The normal Hb amount in the blood is 15g/L. Cyanosis results when deoxygenated Hb over 5g/dL. O2 binding capacity is about 20.1 mL O2/dL. With a decrease in Hb there is a decrease in O2 content of arterial blood but no change in O2 saturation and arterial PO2. O2 delivery to tissue=cardiac output x O2 content of blood.


Oxygen content with CO poisoning

Hb concentration is normal, % O2 sat of Hb decreases (CO competes with O2), dissolved O2 (PaO2) is normal, and total O2 content is decreased.


Oxygen content with anemia

Hb concentration is decreased, % O2 sat of Hb normal, dissolved O2 (PaO2) is normal, and total O2 content is decreased.


Oxygen content with polycythemia

Hb concentration is increased, % O2 sat of Hb normal, dissolved O2 (PaO2) is normal, and total O2 content is increased.


Pulmonary circulation

There is normally a low-resistance, high compliance system. PO2 and PCO2 exert opposite effects on pulmonary and systemic circulation. A decrease in PAO2 causes a hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of lung to well ventilated regions of the lung.


Cor pulmonale

A consequence of pulmonary hypertension is cor pulmonale and subsequent right ventricular failure (jugular venous distention, edema, and hepatomegaly.


Perfusion limited gases

Some gases diffuse so rapidly across the alveolar membrane that their diffusion into blood is only limited by the perfusion of the alveoli. Such gases include O2 (in healthy lungs), CO2, and N2O and are referred to as "perfusion limited." Upon inhalation, these gases equilibrate with the blood early along the total length of the pulmonary capillary, and diffusion can only be increased if blood flow increases. Gases that diffuse slowly across the alveolar membrane and do not equilibrate in the time that the blood traverses the pulmonary capillary are said to be "diffusion limited." Such gases include CO, as well as O2 in the setting of emphysema or pulmonary fibrosis.


Fick's law

The diffusion of gas across the alveolar membrane into the blood can be represented by Fick's law of diffusion: Vgas = (A/T) x Dk x ΔP. A = total diffusing surface area of alveoli. T = alveolar wall thickness. Dk = diffusion constant (based upon the solubility and molecular weight of the gas). ΔP = difference in the partial pressures of the gas across the membrane (P1 - P2)


Pulmonary Vascular Resistance (PVR)

Pulmonary Vascular Resistance (PVR) can be calculated with the following equation: PVR = ( P pulm artery - P left atrium ) / CO. This equation is a derivative of the equation R = ΔP/Q. Ppulm artery = pulmonary artery pressure. Pleft atrium = capillary wedge pressure. CO = cardiac output. R = resistance. Q = flow. ΔP = change in pressure over the length of the vessel. Remember: ΔP = Q x R, so R= ΔP/Q. R=8nl/Pi to the fourth. n = viscosity of blood; 1=vessel length; r=vessel radius.


Alveolar gas equation

The alveolar gas equation is: PAO2 = PiO2 – (PaCO2/R). PAO2 = alveolar PO2 in mmHg. PiO2 = pressure of inspired oxygen in mmHg (can sometimes be approximated to 150). PaCO2 = arterial PCO2 in mmHg. R = respiratory quotient, which = (CO2 produced)/(O2 consumed). The alveolar gas equation allows us to calculate the PAO2 from an arterial blood gas sample, which can be used to ultimately estimate the A-a gradient..


Calculating the pressure of inspired oxygen

When breathing environmental air at sea level, the PiO2 can be approximated to ~150. However, if there is a known altitude change, to calculate the altitude adjusted PiO2: Take the atmospheric pressure (ex: 760 if at sea level) and subtract the H2O vapor pressure (normally ~ 47) which is the moisture added to inspired air as it is humidified by the respiratory mucosa. For example, at sea level this would be: (760 – 47) = 713. Then multiply the result by the FiO2, which is the percentage of O2 in the air (normally 21%). So continuing with the example at sea level, (713) x (.21) = 149.73. Therefore, the FiO2 of room air is 0.21 and the PiO2 of room air is 150 mmHg.


A-a gradient

The A-a gradient is a value that reflects the integrity of oxygen diffusion across the alveolar and pulmonary arterial membranes. The A-a gradient can be calculated by subtracting the arterial partial pressure of oxygen from the alveolar partial pressure of oxygen (PAO2 – PaO2). PAO2 = alveolar oxygen pressure. PaO2 = arterial oxygen pressure. A normal resting A-a gradient in healthy middle aged adults ~ 5-10 mmHg. A-a gradient is normal during conditions of hypoxia caused by Hypoventilation, Decreased FiO2 (experimentally, or at high altitude due to decreased PiO2). Increased A-a gradient may occur in: Shunting, V/Q mismatch, Aging, and Diffusion impairments (ex: interstitial fibrosis or pulmonary edema).



A decrease in PaO2. Causes with a normal A-a gradient include high altitude and hypoventilation (eg opioid use). Causes with an increased A-a gradient includes V/Q mismatch, diffusion limitation, right to left shunt.



A decrease in O2 delivery to tissue. Causes include decreased cardiac output, hypoxemia, anemia, and CO poisoning.



Loss of blood flow. Causes include impeded arterial flow and decreased venous drainage.


V/Q mismatch

Ideally, ventilation is match to perfusion (ie V/Q=1) for adequate gas exchange. Lung zones: V/Q at the apex of lung=3 (wasted ventilation); V/Q at base of lung=0.6 (wasted perfusion). Both ventilation and perfusion are greater at the base of the lung than at the apex of the lung. With exercise (increased cardiac output), there is vasodilation of apical capillaries causes V/Q ratio approaches 1. Certain organisms that thrive in high O2 (eg TB) flourish in the apex.



When V/Q=0, there is an airway (Oirway) obstruction (shunt). In a shunt, 100% O2 does not improve PaO2.


Physiologic dead space

When V/Q=infinity, there is a blood flow obstruction (physiologic dead space). Assuming that there is less than 100% dead space, 100% O2 improves PaO2.


Zone 1 of the lung

It is in the apex. PA is greater than Pa, which is greater than Pv. A slight decrease in V and a large decrease Q causes V/Q to increase.


Zone 2 of the lung

Pa is greater than PA, which is greater than Pv.


Zone 3 of the lung

Pa is greater than Pv, which is greater than PA. A slight increase in V and a large increase in Q causes V/Q to decrease.


CO2 transport

CO2 is transported from tissues to lungs in 3 forms: HCO3 (90%); Carbaminohemoglobin or HbCO2 (5%). CO2 bound to Hb at N-terminus of globin (not heme). CO2 binding favors the taut for (O2 is unlocked); Dissolved CO2 (5%).


Haldane effect

The Haldane effect describes the property of hemoglobin that promotes the release of bound H+ in the presence of increased [O2]. The binding of O2 to hemoglobin makes the Hgb-H+ bond less stable, thus promoting the release of H+. The resulting increase in free [H+] facilitates CO2 formation and expiration at the lungs via the reaction catalyzed by carbonic anhydrase (H+ + HCO3- -> H2CO3 -> CO2 + H2O). This reaction occurs in RBCs. The majority of blood CO2 is carried as HCO3 in the plasma.


Bohr effect

The Bohr effect describes the decrease in hemoglobin's affinity for oxygen in the presence of increased CO2 and decreased pH. This occurs in peripheral tissue.


Response to high altitude

A decrease atmospheric oxygen (PO2) decreases PaO2, which increases ventilation thus decreasing PaCO2). There is also a chronic increase in ventilation. There is an increase in erythropoietin, which increases hematocrit and Hb (chronic hypoxia). It also increases 2,3-BPG, which binds to Hb so that Hb releases more O2. There are cellular changes like increased number of mitochondria. There is an increase in renal excretion of HCO3 to compensate for respiratory alkalosis (can be augment with acetazolamide). Chronic hypoxic pulmonary vasoconstriction results in RVH.


Response to exercise

There is increased CO2 production, increased O2 consumption, and increased ventilation rate to meet O2 demand. V/Q ratio from apex to base becomes more uniform. There is increased pulmonary blood flow due to increased cardiac output. There is also a decrease pH during strenuous exercise (secondary to lactic acidosis). There is no change in PaO2 and PaCO2, but there is an increase in venous CO2 content and a decrease in venous O2 content.



Obstruction of sinus drainage into nasal cavity causing inflammation and pain over affected area (typically maxillary sinuses in adults). The most common acute cause is viral URI, which may cause a superimposed bacterial infection, most commonly S. pneumoniae, H influenzae, M. catarrhalis.



Nose bleed. It most commonly occurs in the anterior segment of the nostril (Kiesselbach plexus). Life threatening hemorrhages occur in the posterior segment (sphenopalatine artery, a branch of maxillary artery).


Deep venous thrombosis

A blood clot within a deep vein causes swelling, redness, warmth, and pain. It is predisposed by Virchow triad (SHE): Stasis. Hypercoagulability (eg defect in the coagulation cascade proteins, such as factor V Leiden. Endothelial damage (exposed collagen triggers clotting cascade). Approximately 95% of pulmonary emboli arise from proximal deep veins of lower extremity. The Homan sign is calf pain with dorsiflexion of the foot. Treatment is unfractionated heparin or low molecular weight heparins (eg enoxaparin) for prophylaxis and acute management. Use oral anticoagulants (eg warfarin, rivaroxaban) for long-term prevention.


Pulmonary emboli

V/Q mismatch causes hypoxemia, which leads to respiratory alkalosis. Symptoms include sudden-onset dyspnea, chest pain, tachypnea, tachycardia. It may also present as sudden death. Lines of Zafn are interdigitating areas of pink (platelets, fibrin) and red (RBCs) found only in the thrombi formed before death, which helps in distinguish pre and postmortem thrombi. Types include Fat, Air, Thrombus, Bacteria, Amniotic fluid, and Tumor. An embolus moves like a FAT BAT. CT pulmonary angiography is imaging test of choice for PE (look for filling defects).


Fat emboli

It is associated with long bone fractures and liposuction. The classic triad is hypoxemia, neurologic abnormalities, and petechial rash.


Air emboli

Nitrogen bubbles precipitate in ascending divers. Treat with hyperbaric O2.


Obstructive lung disease

Obstruction of air flow resulting in air trapping in lungs. Airways close prematurely at high lung volumes, which increases the residual volume and decreases forced vital capacity (FVC). PFTs will show a large decrease in FEV1 and a decrease in FVC, causing the FEV1/FVC ratio to decrease (hallmark, around 70%) and a V/Q mismatch. Chronic , hypoxic pulmonary vasoconstriction can lead to cor pulmonale.


Chronic bronchitis

It is an obstructive lung disease. Blue bloaters. Hyperplasia of mucus secreting glands in the bronchi leads to a Reid index (thickness of gland layer/total thickness of bronchial wall) of less than 50%. Diagnosis is based on a productive cough for over 3 months per year (not necessarily consecutive) for over 2 years. Findings include wheezing crackles, cyanosis (early onset hypoxemia due to shunting), late onset dyspnea, CO2 retention (hypercapnia), and secondary polycythemia.



It is an obstructive lung disease. Pink puffer. There is enlargement of air spaces, decrease in recoil, increase in compliance, decrease in diffusing capacity for CO resulting from destruction of the alveolar walls. There are two types: centriacinar (associated with smoking) and panacinar (associated with alpha 1 antitrypsin deficiency. An increase in elastase activity causes a loss of elastic fibers, thus increasing compliance. Exhalation through pursed lips to increase airway pressure and prevent airway collapse during respiration. There is often a barrel shaped chest.



It is an obstructive lung disease. Bronchial hyperresponsiveness causes reversible bronchoconstriction. There is smooth muscle hypertrophy, Curschmann spirals (shed epithelium forms whorled mucus plugs), and Charcot-Leyden crystals (eosinophilic, hexagonal, double pointed, needle like crystals formed from breakdown of eosinophils in sputum). It can be triggered by viral URIs, allergens, stress. Test with methacholine challenge. Findings include cough, wheezing, tachypnea, dyspnea, hypoxemia, decreased inspiratory/expiratory ratio, pulsus paradoxus, mucus plugging.



It is an obstructive lung disease. Chronic necrotizing infection of bronchi creates permanently dilated airways, purulent sputum, recurrent infections, hemoptysis. It is associated with bronchial obstruction, poor ciliary motility (eg smoking Kartagener syndrome), cystic fibrosis, allergic bronchopulmonary aspergillosis.


Restrictive lung disease

Restricted lung expansion causes a decrease in lung volumes (decrease in FVC and TLC). PFTs will show FEV1/FVC ratio is equal to or over 80%. It can be caused by poor breathing mechanics (extrapulmonary, peripheral hypoventilation, normal A-a gradient). Diseases causing poor muscular effort includes polio or mysthenia gravis. Diseases causing poor structural apparatus include scoliosis or morbid obesity. It can also be due to interstitial lung diseases (decreased diffusing capacity, increased A-a gradient). Such causes include acute respiratory distress syndrome (ARDS), neonatal respiratory distress syndrome (NRDS; hyaline membrane disease), pneumoconioses (eg anthracosis, silicosis, asbestosis), sarcoidosis (bilateral hilar lymphadenopathy, noncaseating granuloma; increased ACE and Ca), idiopathic pulmonary fibrosis (repeated cycles of lung injury and wound healing with increased collagen deposition), Goodpasture syndrome, granulomatosis with polyangiitis (Wegener), langerhans cell histiocytosis (eosinophilic granuloma), hypersensitivity pneumonitis, drug toxicity (bleomycin, busulfan, amiodarone, methotrexate.


Obstructive vs restrictive lung disease

Obstructive lung volumes are greater than normal (increased TLC, increased FRC, increased RV). Restrictive lung volumes are less than normal. In both obstructive and restrictive, FEV1 and FVC are reduced. In obstructive, however, FEV1 is more dramatically reduced compared to FVC, resulting in a decrease in a FEV1/FVC ration.


Hypersensitivity pneumonitis

It is mixed type III/IV hypersensitivity reaction to environmental antigen, causing dyspnea, cough, chest tightness, headache. It is often seen in farmers and those exposed to birds.



Coal workers' pneumoconiosis, silicosis, berylliosis, and asbestosis has an increased risk of cor pulmonale and Caplan syndrome (rheumatoid arthritis and pneumoconioses with intrapulmonary nodules).



It is associated with shipbuilding, roofing, plumbing. Exposure leads to ivory white, calcified, supradiaphragmatic and pleural plaques are pathognomonic of asbestosis. It is associated with an increase incidence of lung cancer (bronchogenic carcinoma is more common than mesothelioma). It affects the lower lobes. Asbestos (ferruginous) bodies are golden-brown fusiform rods resembling dumbbells, found in alveolar septum. Asbestos is from the roof (was common in insulation), but affects the base (lower lobes).



It is associated with exposure to beryllium in aerospace and manufacturing industries. Granulomatous on histology and therefore occasionally responsive to steroids. It affects the upper lobes.


Coal workers' pneumoconioses

Prolonged coal dust exposure creates macrophages laden with carbon causing inflammation and fibrosis. It is also known as black lung disease. It affects the upper lobes.



Anthracosis is an accumulation of carbon dust found in people that live in urban areas where there is air pollution. It is a clinically silent and benign (but frequent) finding on autopsy. It appears as blue-black deposits on the lung surface and in the lymph nodes.



It is associated with foundries, sandblasting, and mines. Macrophages respond to silica and release fibrogenic factors, leading to fibrosis. It is thought that silica may disrupt phagolysosomes and impair macrophages, increasing susceptibility to TB. There is also an increase risk of bronchogenic carcinoma. It affects upper lobes. There are eggshell calcification of hilar lymph nodes. Silica and coal are from the base (earth), but affect the roof upper lobes.


Neonatal respiratory distress syndrome

Surfactant deficiency increases surface tension and leads to alveolar collapse (ground glass appearance of lung fields). A lecithin:sphingomyelin ratio under 1.5 in amniotic fluid is predictive of NRDs. Persistently low O2 tension increases the risk of PDA. Therapeutic supplemental O2 can result inRetinopathy of prematurity, Intraventricular hemorrhage, Bronchopulmonary dysplasia (RIB). Risk factors include prematurity, maternal diabetes (due to an increase in fetal insulin), C-section delivery (decreased release of fetal glucocorticoids). Complications include metabolic acidosis, PDA, necrotizing enterocolitis. Treatment maternal steroids before birth and artificial surfactant for the infant.


Acute respiratory distress syndrome

It is a clinical syndrome characterized by acute onset respiratory failure, bilateral lung opacities, a decrease in PaCO2/FiO2 (the ratio of partial pressure arterial oxygen and fraction of inspired oxygen), with no HF. It may be caused by trauma, sepsis, shock, gastric aspiration, uremia, acute pancreatitis, amniotic fluid embolism. Diffuse alveolar damage increases alveolar capillary permeability causing protein rich leakage into alveoli and noncardiogenic pulmonary edema (normal pulmonary capillary wedge pressure). It results in formation of intra-alveolar hyaline membranes. Initial damages due to release of neutrophilic substances toxic to alveolar wall, activation of coagulation cascade, and oxygen derived free radicals. management includes mechanical ventilation with low tidal volumes and addressing the underlying cause. CXR can show near complete opacification of lungs with obscured cardiomediastinal silhouette.


Sleep apnea

It is defined as repeated cessation of breathing for over 10 seconds during sleep, causing disrupted sleep leading to daytime somnolence. There is normal PaO2 during the day. Nocturnal hypoxia causes systemic/pulmonary hypertension, arrhythmias (atrial fibrillation/flutter), and sudden death. Types include obstructive sleep apnea, central sleep, and obesity hypoventilation sydrome. Hypoxia triggers an increase in EPO release, increasing erythropoiesis.


Obstructive sleep apnea

Respiratory effort against airway obstruction. It is associated with obesity and load snoring. It is caused by excess parapharyngeal tissue in adults, adenotonsillar hypertrophy in children. Treatment includes weight loss, CPAP, surgery.


Central sleep apnea

No respiratory effort due to CNS injury/toxicity.


Obesity hypoventilation syndrome

Obesity (BMI over 30 kg/m2) causes hypoventilation (decreasing the respiratory rate), which decreases PaO2 and increases PaCO2 during sleep. This increases PaCO2 during waking hours (retention).


Pulmonary hypertension

Normal mean pulmonary artery pressure is between 10-14 mmHg. Pulmonary hypertension (PH) over 25 mmHg at rest. It results in arteriosclerosis, medial hypertrophy, intimal fibrosis of pulmonary arteries. At first there is severe respiratory distress, which leads to cyanosis and RVH and can eventually lead to death from decompensated cor pulmonale. There are five classification groups based on cause and treatment. Group 1 is pulmonary arterial hypertension (primary PH). Group 2 is PH due to left heart disease. Group 3 is PH due to chronic lung disease/hypoxia. Group 4 is PH due to chronic thromboembolic disease. Group 5 is PH due to unknown or multifactorial causes (ex: sickle cell anemia)


Pulmonary arterial hypertension (PAH)

Type 1 pulmonary hypertension. It is idiopathic or heritable (often due to an inactivating mutation in BMPR2 gene, which normally inhibits vascular smooth muscle proliferation). There is a poor prognosis. Includes pulmonary venous occlusive disease and persistent PH of newborn. Other causes include drugs (eg amphetamines or cocaine), connective tissue disease, HIV infection, portal hypertension, congenital heart disease, and schistosomiasis.


Pulmonary hypertension due to left heart disease

Type 2 pulmonary hypertension. Causes include systolic.diastolic dysfunction and valvular disease such as mitral stenosis.


Pulmonary hypertension due to lung disease or hypoxia

Type 3 pulmonary hypertension. Destruction of lung parenchyma (eg COPD), hypoxemic vasoconstriction (eg obstructive sleep apnea, living in high altitude).


Chronic thromboembolic pulmonary hypertension

Type 4 pulmonary hypertension. Recurrent microthrombi causes a decrease in cross-sectional area of pulmonary vascular bed.


Multifactorial pulmonary hypertension

Type 5 pulmonary hypertension. Causes include hematologic, systemic, and metabolic disorders.


Physical findings of pleural effusion

Breath sounds are decreased, percussion is dull, fremitus is decreased, and the trachea is either not deviated or deviated away from the side of lesion (if large).


Physical findings of atelectasis (bronchial obstruction)

Breath sounds are decreased, percussion is dull, fremitus is decreased, and the trachea is deviated toward the side of lesion.


Physical findings of simple pneumothorax

Breath sounds are decreased, percussion is hyperresonant, fremitus is decreased, and the trachea is not deviated.


Physical findings of tension pneumothorax

Breath sounds are decreased, percussion is hyperresonant, fremitus is decreased, and the trachea is deviated away from side lesion.


Physical findings of consolidation (lobar pneumonia, pulmonary edema)

There are bronchial breath sounds and late inspiratory crakles, percussion is dull, fremitus is increased, and the trachea is not deviated.


Pleural effusions

Excess accumulation of fluid between pleural layers causes restricted lung expansion during inspiration. It can be treated with thoracentesis to remove fluid. Types include transudate, exudate, lymphatic.



There is a decrease in protein content. It can occur due to increased hydrostatic pressure or decreased oncotic pressure (eg HF, nephrotic syndrome, hepatic cirrhosis).



There is an increase in protein content, cloudy. It occurs due to malignancy, pneumonia, collagen vascular disease, trauma (occurs in state of increased vascular permeability). It must be drained due to a risk of infection.


Lymphatic effusion

It is also known as chylothorax. It occurs due to thoracic duct injury from trauma or malignancy. It is milky appearing fluid. There are also increased triglycerides.



Accumulation of air in pleural space. It causes unilateral chest pain and dyspnea, unilateral chest expansion, decreased tactile fremitus, hyperresonance, diminished breath sounds, all on the affected side.


Primary spontaneous pneumothorax

It occurs due to rupture of apical blebs or cysts. It occurs most frequently in tall, thin young males.


Secondary spontaneous pneumothorax

It occurs due to diseased lung (eg bullae in emphysema, infections), mechanical ventilation wit use of high pressures, which can cause barotrauma.


Traumatic pneumothorax

It is caused by blunt (eg rib fracture) or penetrating (eg gunshot) trauma.


Tension pneumothorax

It can be any of the types of pneumothorax. Air enters the pleural space but cannot exit. The increasing trapped air lead to tension pneumothorax. Trachea deviates away from affected lung.


Lobar pneumonia

Typical organisms include S. pneumoniae most frequently, also Legionella, Klebsiella. Characteristics include intra-alveolar exudate causes consolidation. It may involve entire lobe or long.



Typical organisms include S. pneumoniae, S. aureus, H. influenzae, Klebsiella. Characteristics include acute inflammatory infiltrates from bronchioles into adjacent alveoli. There is also patchy distribution involving a lobe or more.


Interstitial (atypical) pneumonia

Typical organisms include viruses (influenza, CMV, RSV, adenoviruses), Mycoplasma, Legionella, Chlamydia. Characteristics include diffuse patchy inflammation localized to interstitial areas at alveolar walls. There is diffuse distribution involving 1 lobe or more. It generally follows a more indolent course (walking pneumonia).


Lung abscess

It is localized collection of pus within parenchyma. It is caused by aspiration of oropharyngeal contents (especially in patients predisposed to loss of consciousness [eg alcoholics, epileptics]) or bronchial obstruction (eg cancer). Treatment is clindamycin. Air fluid levels are often seen on CXR. Fluid levels are common in cavities and their presence suggests cavitation. It is often due to anaerobes (eg Bacteroides, Fusobacterium, Peptostreptococcus) or S. aureus.



Malignancy of the pleura is associated with asbestosis. It may result in hemorrhagic pleural effusion (exudative), pleural thickening. Psammoma bodies are seen on histology. Smoking is not a risk factor.


Pancoast tumor (superior sulcus tumor)

Carcinoma that occurs in apex of the lung may cause Pancoast syndrome by invading cervical sympathetic chain, causing Horner syndrome (ipsilateral ptosis, miosis, anhidrosis), SVC syndrome, sensorimotor deficits, and hoarseness.


Superior vena cava syndrome

An obstruction of the SVC that impairs blood drainage from the head (facial plethora with blanching after applying pressure), neck (jugular venous distention), and upper extremities (edema). It is commonly caused by malignancy (eg Pancoast tumor) and thrombosis from indwelling catheters. This is a medical emergency. It can raise intracranial pressure (if obstruction is severe) causing headaches, dizziness, and an increased risk of aneurysm/rupture of intracranial arteries.


Lung cancer

It is the leading cause of cancer death. It can present with cough, hemoptysis, bronchial obstruction, wheezing, pneumonic "coin" lesion on CXR or noncalcified nodule on CT. Sites of metastases from lung cancer include the adrenals, brain, bone (pathologic fracture), liver (jaundice, hepatomegaly). In the lung, metastases (usually multiple lesions) are more common than primary neoplasms. Metastases come from the breast, colon, prostate, and bladder cancer. Complications include (SPHERE): Superior vena cava syndrome, Pancoast tumor, Horner syndrome, Endocrine (paraneoplastic), Recurrent laryngeal nerve compression (hoarseness), and Effusions (pleural or pericardial). Risk factors include smoking, secondhand smoke, radon, asbestos, family history. Squamous and Small cell carcinoma are Sentral (central).


Small cell (oat cell) carcinoma

The location of the tumor is most often central. It is undifferentiad and very aggressive. It may produce ACTH (Cushing syndrome), SIADH, or Antibodies against presynaptic Ca channels (Lamber Eaton myasthenic syndrome) or neurons (paraneoplastic myelitis/encephalitis). Amplification of myc oncogenes is common. They are inoperable, treat with chemotherapy. They are neoplasms of neuroendocrine Kulchitsky cells, which appear as small dark blue cells. It stains as Chromogranin A positive.



The location of the tumor is most often peripheral. It is the most common lung cancer in nonsmokers and overall (except for metastases). Activating mutations include KRAS, EGFR, and ALK. It is associated with hypertrophic osteoarthropathy (clubbing). Bronchioloalveolar subtype (adenocarcinoma in situ): CXR often shows hazy infiltrates similar to pneumonia. It has an excellent prognosis. On histology, there is a glandular pattern and often stains mucin positive. Bronchioalveolar subtype grows along alveolar septa causing an apparent thickening of alveolar walls.


Squamous cell carcinoma

The location of the tumor is most often Central. A hilar mass arises from the bronchus. There is also Cavitation. Smoking Cigarettes is a risk factor. There can also be hyperCalcemia due to PTHrP production. Histology will show keratin pearls and intercellular bridges.


Large cell carcinoma

The location of the tumor is most often peripheral. It is highly anaplastic undifferentiated tumor. There is a poor prognosis. It is less responsive to chemotherapy and is removed surgically. Histology will show pleomorphic giant cells that can secrete beta-hCG.


Bronchial carcinoid tumor

It has excellent prognosis, metastasis is rare. Symptoms are usually due to mass effect. It can occasionally cause carcinoid syndrome (5-HT secretion causes flushing, diarrhea, and wheezing). Histology will show nests of endocrine cells. Like small cell carcinoma, it stains chromogranin A positive.


H1 blockers

They are reversible inhibitors of H1 histamine receptors.


First generation H1 blockers

Diphenhydramine, dimenhydrinate, chlorpheniramine. Names contain -en/-ine or -en/-ate. They are used to treat allergy, motion sickness, sleep aid.


Toxicity of first generation H1 blockers

Sedation, antimuscarinic, anti alpha adrenergic.



First generation H1 blockers



First generation H1 blockers



First generation H1 blockers


Second generation H1 blockers

Loratadine, fexofenadine, desloratadine, certirizine. Names usually end with -adine. They are used to treat allergies.


Toxicity of second generation H1 blockers

It is far less sedating than 1st generation because of decrease entry into CNS.



Second generation H1 blockers



Second generation H1 blockers



Second generation H1 blockers



Second generation H1 blockers



Includes guaifenesin and N-acetylcysteine.



It is an expectorants that thins respiratory secretions. It does not suppress cough reflex.



It is a mucolytic that can loosen mucous plugs in CF patients by disrupting disulfide bonds. It is also used as an antidote for acetaminophen overdose.



Antitussive (antagonizes NMDA glutamate receptors). It is a synthetic codeine analog. It has a mild opioid effect when used in excess. Naloxone can be given for overdose. It has mild abuse potential. It may cause serotonin syndrome if combined with other serotenergic agents.



It is an alpha adrenergic agonists and is used as a nasal decongestants. It is used to reduce hyperemia, edema, nasal congestion. It is also used to open obstructed eustachian tubes. Pseudoephedrine is also used illicitly to make methamphetamine. Toxicities include hypertension and CNS stimulation/anxiety.



It is an alpha adrenergic agonists and is used as a nasal decongestants. It is used to reduce hyperemia, edema, nasal congestion. It is also used to open obstructed eustachian tubes. Toxicities include hypertension.


Pulmonary hypertension drugs

Endothelin receptor antagonists, PDE-5 inhibitors, prostacyclin analogs.


Endothelin receptor antagonists

It is used to treat pulmonary hypertension. It includes bosentan. It competitively antagonize endothelin-1 receptors, which decreases pulmonary vascular resistance. Hepatotoxic (monitor LFTs).


PDE-5 inhibitors

It is used to treat pulmonary hypertension. It includes sildenafil. It inhibits cGMP PDE5 and prolong vasodilatory effect of nitric oxide. It is also used to treat erectile dysfunction.


Prostacyclin analogs

It is used to treat pulmonary hypertension. It includes epoprostenol, iloprost. Prostacyclins (PGI2) with direct vasodilatory effect on pulmonary and systemic arterial vascular beds. It inhibits platelet aggregation. Side effects include flushing and jaw pain.



Endothelin receptor antagonists



PDE-5 inhibitors



Prostacyclin analogs



Prostacyclin analogs


Asthma drugs

Bronchoconstriction is mediated by inflammatory processes and parasympathetic tone. Therapy is directed as these 2 pathway.s


Beta 2 agonists

Includes albuterol, salmeterol, formoterol.



A beta 2 agonists that is used to treat asthma. It relaxes bronchial smooth muscle (beta 2). It is used during an acute exacerbation.



It is a long acting beta 2 agonists that is used as a prophylaxis asthma treatment. Adverse effects include tremor and arrhythmia.



It is a long acting beta 2 agonists that is used as a prophylaxis asthma treatment. Adverse effects include tremor and arrhythmia.



It is used to treat asthma. Includes flutixasone and budesonide. It inhibits the synthesis of virtually all cytokines. It inactivates NF-kB, the transcription factor that induces production of TNF-alpha and other inflammatory agents. It is the first line therapy for chronic asthma









It is competitively blocks muscarinic receptors, preventing bronchoconstriction. It is also used for COPD. Tiotropium is long acting.



Long acting muscarinic antagonists



Includes montelukast, zafirlukast, and zileuton.



It blocks leukotrienes receptors (CysLT1). It is especially good for aspirin-induced asthma.



It blocks leukotrienes receptors (CysLT1). It is especially good for aspirin-induced asthma.



5-lipoxygenase pathway inhibitor, which blocks conversion of arachidonic acid to leukotrienes. It can be hepatotoxic.



It is a monoclonal anti-IgE antibody. It binds mostly unbound serum IgE and blocks binding to FcERI. It is used in allergic asthma resistant to inhaled steroids and long-acting beta 2 agonists.



Methylzanthines. It likely causes bronchodilation by inhibiting phorphodiesterase, which increases cAMP levels due to a decrease in cAMP hydrolysis. Its usage is limited because of a narrow theraputic index (cardiotoxicity, neurotoxicity). It is metabolized by cytochrome P450. It blocks the actions of adenosine.



Muscarinic receptor (M3) agonist. It is used in bronchial challenge test to diagnose asthma.