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Flashcards in Respiratory Deck (81):

Respiratory Tree

1. Conducting Zone
2. Respiratory Zone


Conducting Zone

-large airways consist of nose, pharynx, trachea, & bronchi
-small airways consist of bronchioles & terminal bronchioles
-warms, humidifies, & filters air but does not participate in gas exchange, "anatomic dead space"
-Extending to end of bronchi: cartilage, goblet cells
-Extending to end of terminal bronchioles:
pseudostratified ciliated columnar cells (beat mucus up & out of lungs)
smooth muscle of the airway walls (sparse beyond this point)


Respiratory Zone

-lung parenchyma; consists of respiratory bronchioles, alveolar ducts, & alveoli, participates in gas exchange
-mostly cuboidal cells in respiratory bronchioles, then simple squamous cells up to alveoli. No cilia
-alveolar macrophages clear debris & participate in immune response


Pneumocytes: Type I cells

-97% of alveolar surfaces, line the alveoli
-squamous; thin for optimal gas diffusion


Pneumocytes: Type II Cells

-Secrete pulmonary surfactant, dec. alveolar surface tension & prevention of alveolar collapse (atelectasis).
-cuboidal & clustered
-also serve as precursors to type I cells & other type II cells
-type II cells proliferate during lung damage


Pneumocytes: Clara Cells

-Nonciliated; columnar with secretory granules
-secrete component of surfactant; degrade toxins, act as reserve cells


Pneumocytes: Collapsing Pressure

pressure = P = 2(surface tension)/radius
-alveoli have inc. tendency to collapse on expiration as radius dec. (law of Laplace)
-Pulmonary surfactant is a complex mix of lecithins, the most important of which is dipalmtoylphosphatidylcholine
-surfactant synthesis begins around week 26 of gestation, but mature levels are not achieved until around week 35
-A lecithin-to-sphingomyelin ratio >2.0 in amniotic fluid indicated fetal lung maturity


Lung Lobe Relationships

-Right lung has 3 lobes, Left has 2 Lobes & Lingula (homologue of right middle lobe)
-Right lung is more common site for inhaled foreign body b/c the right main stem bronchus is wider & more vertical than the left
Aspirate a peanut: upright-lower portion of right inferior lobe, supine-superior portion of right inferior lobe
-instead of middle lobe, the left lung has a space occupied by the heart
-the relation of the pulmonary artery to the bronchus as each lung hilus is described by RALS (right anterior, left superior)


Diaphragm Structures

-structures perforating diaphragm
T10: Esophagus, vagus (2 trunks)
T12: aorta, thoracic duct, azygos vein
-Diaphragm is innervated by C3,4,5 (phrenic)
-pain from the diaphragm can be referred to the shoulder (C5) and the trapezius ridge (C3,4)


Muscles of Respiration

Quite Breathing
-Inspiration: diaphragm
-Expiration: passive
-Inspiration: external intercostals, scalene muscles, sternocleidomastoids
-Expiration: rectus abdominis, internal/external obliques, transversus abdominis, internal intercostals


Inspiratory Reserve Volume

-air that can still be breathed in after normal inspiration


Tidal Volume

-air that moves into lung with each quiet inspiration


Expiratory Reserve Volume

-air that can still be breathed out after normal expiration


Residual Volume

-air in lung after maximal expiration; cannot be measured on spirometry


Inspiratory Capacity



Functional Residual Capacity

RV + ERV (volume in lungs after normal expiration)


Vital Capacity (VC)

-maximum volume of gas that can be expired after a maximal inspiration


Total Lung Capacity

= IRV + TV + ERV + RV
-volume of gas present in lungs after a maximal inspiration


Determination of physiologic dead space

Vd = Vt x (Paco2 - Peco2)/ Paco2

Vd = physiological dead space = anatomical dead space of conducting airways plus functional dead space in alveoli; apex of healthy lung is largest contributor of functional dead space
-volume of inspired air that does not take part in gas exchange
Vt = tidal volume
Paco2 = arterial Pco2, Peco2 = expired air Pco2
Taco, PAco, PEco, PAco


Lung & Chest Wall

-tendency for lungs to collapse inward chest wal to spring outward
-at FRC, inward pull off lung is balanced by outward pull of chest wall, and system pressure is atmospheric
-at FRC, airway & alveolar pressures are 0, & intrapleural pressure is negative (prevents pneumothorax)
-Compliance - change in lung volume for a give change in pressure; dec. in pulmonary fibrosis, pneumonia, & pulmonary edema; inc. in emphysema and normal aging



-hemoglobin is composed of 4 polypeptide subunits (2 alpha and 2 beta) and exists in 2 forms:
-T (taut) form has low affinity for O2
-R (relaxed) form has high affinity for O2 (300x) hemoglobin exhibits positive cooperativity & negative allostery
-inc. Cl-, H+, CO2, 2-3BPG, & temp favor taught form over relaxed form (shifts dissociation curve to right, leading to inc. O2 unloading)
-fetal hemoglobin (2alpha & 2 gamma subunits) has lower affinity for 2-3-BPG than adult hemoglobin & thus has higher affinity for O2
-Taut in Tissues, Relaxed in Respiratory


Hemoglobin Modifications

Lead to tissue hypoxia from dec. O2 saturation and dec. O2 content



-oxidized form of hemoglobin (ferric, Fe3+) that does not bind 02 as readily, but had inc. affinity for cyanide
-Fe in hemoglobin is normally in reduced state (ferrous, Fe2+)
-to treat cyanide poisoning, use nitrates to oxidize hemoglobin to methemoglobin, which binds cyanide, allowing cytochrome oxidase to function
-use thiosulfate to bind this cyanide, forming thiocyanate, which is renally excreted
-Methemoglobinemia can be treated w/methylene blue
-nitrates cause poisoning by oxidizing Fe2+ to Fe3+



-form of hemoglobin bound to CO in place of O2
-caused dec. oxygen-binding capacity with a left shift in the oxygen-hemoglobin dissociation curve
-dec. oxygen unloading in tissues
-CO has 200x greater affinity than O2 for hemoglobin


Oxygen-hemoglobin Dissociation Curve

-sigmoidal shape due to positive cooperativity (tetrameric hemoglobin molecule can bind 4 oxygen molecules & has higher affinity for each subsequent oxygen molecule bound)
-myoglobin is monomeric & thus does not show positive cooperativity, curve lacks sigmoidal appearance
-when curve shifts to the right, dec. affinity of hemoglobin for O2 (facilities unloading of O2 to tissues)
-an inc. in all factors (except pH) causes a shift of the curve to the right
-a dec. in all factors (except pH) causes a shift of the curve to the left
-fetal Hb has a higher affinity for oxygen than adult Hb, so its dissociation curve is shifted left

Right shift: CO2, BPG (2,3-BPG), Exercise, Acid/Altitude, Temp.


Pulmonary Circulation

-normally low-resistance, high-compliance system
-PO2 & PCO2 exert opposite effects on pulmonary & systemic circulation
-a dec. in PAO2 causes a hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung
-Perfusion Limited-02 (normal health), CO2 & N20, gas equilibrates early along the length of the capillary, diffusion can be inc. only if blood flow inc.
-Diffusion Limited-O2 (emphysema, fibrosis), CO, gas does not equilibrate by the time blood reaches the end of the capillary
-a consequence of pulm. HTN is cor pulmonale & subsequent right ventricular failure (jugular venous distention, edema, hepatomegaly)


Pulmonary Circulation Diffusion

Vgas = A/T X Dk(P1-P2) wehre A = area, T=thickness, Dk (P1-P2) ~ difference in partial pressures
-A dec. in emphysema
-T inc. in pulmonary fibrosis


Pulmonary HTN

Normal pulmonary artery pressure = 10-14 mmHg; pulmonary HTN >25 mmHg or > 35mmHg during exercise
-results in arteriosclerosis, medial hypertrophy, & intimal fibrosis of pulmonary arteries
Course: severe respiratory distress, cyanosis & RVH, death from decompensated cor pulmonale


Primary Pulmonary HTN

-due to an inactivating mutation in the BMPR2 gene (normally functions to inhibit vascular smooth muscle proliferation); poor prognosis


Secondary Pulmonary HTN

-due to COPD (destruction of lung parenchyma); mitral stenosis (inc. resistance, inc. pressure), recurrent thromboemboli (dec. cross-sectional area of pulmonary vascular bed); autoimmune disease (systemic sclerosis; inflammation, intimal fibrosis, medial hypertrophy); left-to-right shunt (inc. shear stress, endothelial injury); sleep apnea or living at high altitude (hypoxic vasoconstriction)


Pulmonary Vascular Resistance

PVR = P (pulmonary artery) - P (L atrium) / cardiac output
change in P = Q X R
R = 8nl/pir^4


Oxygen content of Blood

O2 content = (O2 binding capacity x % saturation) + dissolved 02
-normally 1g Hb can bind 1.34 mL O2; normal Hb amount in blood is 15g/dL, cyanosis results when deoxygenated Hb > 5g/dL
-O2 binding capacity ~ 20.1mL O2/dL
-O2 content of arterial blood dec. as Hb falls, but O2 saturation & arterial PO2 do not
-Oxygen delivery to tissues = cardiac output x oxygen content of blood


Alveolar Gas Equation

PAO2 = PIO2 - PaCO2/R
-can normally be approximated
PAo2 = 150 - PaCO2/0.8
PAO2 = alvolar PO2 (mmHg)
PIO2 = PO2 in inspired air (mmHg)
PaCO2 = arterial PCO2 (mmHg)
R = respiratory quotient = CO2 produced/O2 consumed
A-a gradient = PAO2 - PaO2 = 10-15mmHg
-inc. A-a gradient may occur in hypoxemia; causes include shunting, V/Q mismatch, fibrosis (impairs diffusion)



dec. PaO2
-normal A-a gradient (high altitude, hypoventilation)
-inc. A-a gradient (V/Q mismatch, diffusion limitation, right-to-left shunt)



dec. O2 delivery to tissue
-dec. cardiac output
-CO poisoning



loss of blood flow
-impeded arterial flow
-reduced venous drainage


V/Q Mismatch

-Ideally, ventilation is matched to perfusion (V/Q = 1) in order for adequate gas exchange to occur
-Lung zones:
Apex of lung = V/Q = 3 (wasted ventilation)
Base of lung = V/6 = 0.6 (wasted perfusion)
-both ventilation & perfusion are greater at the base of the lung than at the apex of the lung
-with exercise (inc. cardiac output), there is vasodilation of apical capillaries, resulting in a V/Q ratio that approaches 1
-certain organisms that thrive in high O2 (TB) flourish in the apex
-V/Q to 0 = airway obstruction (shunt), in shunt 100% O2 does not improve PO2
-V/Q to infinity = blood flow obstruction (physiologic dead space) assuming < 100% dead space, 100% O2 improves PO2


CO2 Transport

-carbon dioxide is transported from tissue to the lungs in 3 forms
1) bicarb (90%)
2) carbaminohemoglobin or HbCO2 (5%), CO2 bound to hemoglobin at N-terminus of globin (not heme). CO2 binding favors taut form (O2 unloaded)
3) dissolved CO2 (5%)
-in lungs, oxygenation of Hb promotes dissociation of H+ from Hb. This shifts equilibrium toward CO2 formation; therefore CO2 is released from RBCs (Haldane effect)
-In peripheral tissue, inc. H+ from tissue metabolism shifts curve to right, unloading O2 (Bohr effect)
-Majority of blood CO2 is carried as bicarbonate in the plasma


Breathing/Lung Response to High Altitude

-Acute inc. in ventilation, dec. PO2 & PCO2
-inc. O2 consumption
-inc. ventilation rate to meet O2 demand
-V/Q ratio from apex to base becomes more uniform
-inc. pulmonary blood flow due to inc. cardiac output
-dec. pH during strenuous exercise (secondary to lactic acidosis)
-no change in PaO2 & PaCO2, but inc. in venous CO2 content & dec. in venous O2 content


Deep Venous Thrombosis

-Predisposed by Virchow's Triad
1) stasis
2) hypercoagulability (defect in coagulation cascade proteins, most commonly factor V Leiden)
3) Endothelia damage (exposed collagen triggers clotting cascade)
-can lead to pulmonary embolus
-Homan's sign-dorsiflexion of foot, calf pain
-Use heparin for prevention & acute management; use warfarin for long-term prevention of DVT recurrence


Pulmonary Emboli

-Sudden-onset dyspnea, chest pain, tachypnea
-May present as sudden death
-Types: Fat, Air, Thrombus, Bacteria, Amniotic fluid, Tumor
Fat: associated w/long bone fractures & liposuction; classic triad of hypoxemia, neurologic abnormalities, and petechial rash
-Amniotic fluid emboli-can lead to DIC, especially postpartum
-An embolus moves like a FAT BAT
-Approx. 95% of pulmonary emboli arise from deep leg veins
-CT pulmonary angiography is the imaging test of choice for a PE


Obstructive Lung Disease

-obstruction of air flow resulting in air trapping in the lungs
-airways close prematurely at high lung volumes, resulting in inc. RV and dec. FVC
-PFTs: dec. FEV1, dec. FVC, dec. FEV1/FCV ratio (hallmark), V/Q mismatch


Chronic Bronchitis

Obstructive Lung Disease
"blue bloaters"
-a form of COPD along with emphysema
-hypertrophy of mucus-secreting glands in the bronchi, Reid index (thickness of gland layer/total thickness of bronchial wall) > 50%
-productive cough for > 3 months per year (not necessarily consecutive) for > 2 years, disease of small airways
-Findings: wheezing, crackles, cyanosis (early onset hypoxemia due to shunting), late-onset dyspnea



Obstructive Lung Disease
"Pink puffer" barrel-shaped chest
-enlargement of air spaces and dec. recoil resulting from destruction of alveolar walls; inc. compliance
2 Types:
1) centricinar- associated with smoking
2) panacinar- associated with alpha-1antitrypsin deficiency
-inc. elastase activity
-inc. lung compliance due to loss of elastic fibers
-exhalation through pursed lips to inc. airway pressure & prevent airway collapse during respiration



Obstructive Lung Disease
-Bronchial hyperresponsiveness causes reversible bronchoconstriction. Smooth muscle hypertrophy, Curschmann's spirals (shed epithelium forms mucus plugs), and Charcot-Leyden crystals (formed from breakdown of eosinophils in sputum)
-can be triggered by viral URIs, allergens, & stress
-Test with methacholine challenge
-Finding: cough, wheezing, tachypnea, dyspnea, hypoxemia, dec. I/E ration, pulsus paradoxus, mucus plugging



Obstructive Lung Disease
-Chronic necrotizing Infection of bronchi, permanently dilated airways, purulent sputum, recurrent infections, hemoptysis
-associated with bronchial obstruction, poor ciliary motility (smoking), Kartagener's syndrome, cystic fibrosis, allergic bronchopulmonary aspergillosis


Restrictive Lung Disease

-restricted lung expansion causes dec. lung volumes (dec. FVC and TLC)
-PFTs - FEV1/FVC ratio > 80%
1) poor breathing mechanics (extrapulmonary hypoventilation, normal A-a gradient)
-poor muscular effort-polio, myasthenia gravis
-poor structural apparatus-scoliosis, morbid obesity
2) Interstitial Lung Diseases (pulmonary, lowered diffusing capacity, inc. A-a gradient)
-acute respiratory distress syndrome (ARDS)
-neonatal respiratory distress syndrome (hyalin membrane disease)
-sarcoidosis: bilateral hilar lymphadenopathy, noncaseating granuloma, inc. ACE & Ca
-idiopathic pulmonary fibrosis (repeated cycles of lung injury & wound healing w/inc. collagen deposition)
-Goodpasture's syndrome
-Granulomatosis with polyangiitis (Wegener's)
-Langerhans cell histiocytosis (eosinophilic granuloma)
-Hypersensitivity pneumonitis
-Drug toxicity (bleomycin, busulfan, amiodarone, methotrexate)



-anthracosis, silicosis, & asbestosis, inc. risk of cor pulmonale & Caplan's syndrome



-associated with coal mines "coal miner's lung"
-affects upper lobe



-associated with foundries, sandblasting, & mines
-macrophages respond to silica & release fibrinogenic factors, leading to fibrosis.
-it is thought that silica may disrupt phagolysosomes & impair macrophages, increasing susceptibility to TB
-also increases risk of bronchogenic carcinoma
-affects upper lobes
-"eggshell" calcification of hilar lymph nodes



-associated with shipbuilding, roofing, & plumbing
-"Ivory white" calcified pleural plaques are pathognomonic of asbestos exposure, but are not precancerous
-associated with an inc. risk of bronchogenic carcinoma & mesothelioma
-affects lower lobes
-asbestos bodies are golden-brown fusiform rods resembling dumbbells


Neonatal Respiratory Distress Syndrome

-surfactant deficiency leading to inc. surface tension, resulting in alveolar collapse
-a lecithin: sphingomyelin ration<1.5 in amniotic fluid is predictive of neonatal respiratory distress syndrome
-persistently low O2 tension, risk of PDA
-therapeutic supplemental O2 can result in retinopathy of prematurity & bronchopulmonary dysplasia
-Risk factors: prematurity, maternal diabetes (due to elevated fetal insulin), cesarean delivery (dec. release of fetal glucocorticoids)
-Treatment: maternal steroids b/f birth, artificial surfactant for infants


Acute Respiratory Distress Syndrome (ARDS)

-may be caused by trauma, sepsis, shock, gastric aspiration, uremia, acute pancreatitis, or amniotic fluid embolism
-diffuse alveolar damage, inc. alveolar capillary permeability, protein-rich leakage into alveoli
-results in formation of intra-alveolar hyaline membrane
-initial damage due to release of neutrophilic substances toxic to alveolar wall, activation of coagulation cascade, & oxygen-derived free radicals


Obstructive vs. Restrictive Lung Disease

normal FEV1/FVC = 80%
obstructive FEV1/FVC < 80%
restrictive FEV1/FVC > 80%


Sleep Apnea

-repeated cessation of breathings > 10 sec during sleep, disrupted sleep, daytime somnolence
Central Sleep Apnea: no respiratory effort
Obstructive Sleep Apnea: respiratory effort against airway obstruction. Associated with obesity, loud snoring, systemic/pulmonary HTN, arrhythmias, & possibly sudden death
-Treatment: weight loss, CPAP, surgery
Hypoxia, inc. EPO release, inc. erythropoiesis


Lung Physical Findings: Pleural Effusion

Breath sounds: dec.
Percussion: Dull
Fremitus: dec.
Tracheal Deviation: none


Lung Physical Findings: Atelectasis

bronchial obstruction
Breath sounds: dec.
Percussion: Dull
Fremitus: dec.
Tracheal Deviation: toward side of lesion


Lung Physical Findings: Spontaneous Pneumothorax

Breath sounds: dec.
Percussion: hyperresonant
Fremitus: dec.
Tracheal Deviation: toward side of lesion


Lung Physical Findings: Tension Pneumothorax

Breath sounds: dec.
Percussion: hyperresonant
Fremitus: dec.
Tracheal Deviation: away from lesion


Lung Physical Findings: Consolidation

(lobular pneumonia, pulmonary edema)
Breath sounds: bronchial breath sounds; late inspiratory crackles
Percussion: Dull
Fremitus: inc
Tracheal Deviation: none


Lung Cancer

-leading cause of cancer death
-presentation: cough, hemoptysis, bronchial obstruction, wheezing, pneumonic "coin" lesion on x-ray film or noncalcified nodule on CT
-metastatic cancer is most common cause, most often from breast, colon, prostate, & bladder cancer
-sites of metastases: adrenals, brain, bone (pathologic fracture), liver (jaundice, hepatomegaly)
SPHERE of complications:
Superior vena cava syndrome
Pancoast tumor
Horner's Syndrome
Endocrine (paraneoplastic)
Recurrent laryngeal symptoms (hoarseness)
Effusions (pleural or pericardial)
-all lung cancer types except bronchioloalveolar and bronchial carcinoid are associated with smoking


Lung Cancer: Adenocarcinoma

Location: peripheral
-most common lung cancer in nonsmokers & females
-activating mutations in k-ras common
-associated with hypertrophic osteoarthropathy (clubbing)
-bronchioloalveolar subtype: CXR often shows hazy infiltrates similar to pneumonia; excellent prognosis
-bronchioloalveolar subtype: grows along alveolar septa, apparent "thickening" of alveolar walls


Lung Cancer: Squamous Cell Carcinoma

Location: central
-hilar mass arising from bronchus: Cavitation; Cigarettes; hyperCalcemia (produces PTHrP)
-Keratin pearls & intercellular bridges


Lung Cancer: Small Cell Carcinoma

Oat cell
Location: central
-undifferentiated, very aggressive
-may produce ACTH, ADH, or Abs against presynaptic Ca channels (Lambert-Eaton syndrome)
-Amplification of myc oncogenes common
-inoperable, treated with chemo
-neoplasm of neuroendocrine Kulchitsky cells, small dark blue cells


Lung Cancer: Large Cell Carcinoma

Location: Peripheral
-highly anaplastic undifferentiated tumor; poor prognosis
-less responsive to chemo, removed surgically
-pleomorphic giant cells


Lung Cancer: Bronchial Carcinoid Tumor

-Excellent prognosis, metastasis rare
-Symptoms usually due to mass effect; occasionally carcinoid syndrome (serotonin secretion: flushing, diarrhea, wheezing)
-nests of neuroendocrine cells; chromogranin +


Lung Cancer: Mesothelioma

Location: pleural
-Malignancy of the pleura associated with asbestosis
-Results in hemorrhagic pleural effusions & pleural thickening
-Psammoma bodies


Pancoast Tumor

-Carcinoma that occurs in apex of lung may affect cervical sympathetic plexus, causing Horner's Syndrome


Horner's Syndrome

-ipsilateral ptosis, miosis, anhidrosis


Superior Vena Cava Syndrome

-an obstruction of the SVC that impairs blood drainage from the head "facial plethora," neck (jugular venous distention), and upper extremities (edema).
-Commonly caused by malignancy & thrombosis from indwelling catheters
-Medical emergency
-Can raise intracranial pressure (if obstruction severe)-headaches, dizziness, and inc. risk of aneurysm/rupture of cranial arteries


Lobular Pneumonia

S. pneumoniae most frequently, Klebsiella
-intra-alveolar exudate - consolidation; may involve entire lung


Bronchopneumonia Pneumonia

S. pneumoniae, S. aureus, H. influenzae, Klebsiella
-Acute inflammatory infiltrates from bronchioles into adjacent alveoli; patchy distribution involving > 1 lobe


Interstitial (atypical) Pneumonia

viruses (influenza, RSV, adenoviruses), Mycoplasma, Legionella, Chlamydia
-Diffuse patchy inflammation localized to interstitial areas at alveolar walls; distribution involving > 1 lobe
-generally follows a more indolent course


Lung Abscess

-localized collection of pus within parenchyma
-Caused by: bronchial obstruction (cancer); aspiration of oropharyngeal contents (especially in patients predisposed to loss of consciousness. (alcoholics or epileptics)
-air-fluid levels often seen on CXR
-often due to S. aureus or anaerobes (bacteroides, Fusobacterium, Peptostreptococcus)


Hypersensitivity Pneumonitis

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


Pleural Effusions: Transudate

-dec. protein content
-due to CHF, nephrotic syndrome, or hepatic cirrhosis


Pleural Effusions: Exudate

-inc. protein content, cloudy
-due to malignancy, pneumonia, collagen vascular disease, trauma (occurs in states of inc. vascular permeability)
-must drain in light of risk of infectoin


Pleural Effusions: Lymphatic

-also known as chylothorax
-due to thoracic duct injury from trauma, malignancy
-milky-appearing fluid, inc. triglycerides



unilateral chest pain & dyspnea, unilateral chest expansion, dec. tactile fremitus, hyperresonance, diminished breath sounds


Spontaneous Pneumothorax

-Accumulation of air in the pleural space
-Occurs most frequently in tall, thin, young males because of rupture of apical blebs
-Trachea deviates toward affected lung


Tension Pneumothroax

-Usually occurs in setting of trauma or lung infection
-Air is capable of entering pleural space but not exiting
-Tracheal deviates away from affected lung