Respiratory Flashcards
(81 cards)
1
Q
Respiratory Tree
A
- Conducting Zone
2. Respiratory Zone
2
Q
Conducting Zone
A
-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)
3
Q
Respiratory Zone
A
- 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
4
Q
Pneumocytes: Type I cells
A
- 97% of alveolar surfaces, line the alveoli
- squamous; thin for optimal gas diffusion
5
Q
Pneumocytes: Type II Cells
A
- 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
6
Q
Pneumocytes: Clara Cells
A
- Nonciliated; columnar with secretory granules
- secrete component of surfactant; degrade toxins, act as reserve cells
7
Q
Pneumocytes: Collapsing Pressure
A
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
8
Q
Lung Lobe Relationships
A
-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)
9
Q
Diaphragm Structures
A
-structures perforating diaphragm
T8: IVC
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)
10
Q
Muscles of Respiration
A
Quite Breathing
-Inspiration: diaphragm
-Expiration: passive
Exercise
-Inspiration: external intercostals, scalene muscles, sternocleidomastoids
-Expiration: rectus abdominis, internal/external obliques, transversus abdominis, internal intercostals
11
Q
Inspiratory Reserve Volume
A
-air that can still be breathed in after normal inspiration
12
Q
Tidal Volume
A
-air that moves into lung with each quiet inspiration
~500mL
13
Q
Expiratory Reserve Volume
A
-air that can still be breathed out after normal expiration
14
Q
Residual Volume
A
-air in lung after maximal expiration; cannot be measured on spirometry
15
Q
Inspiratory Capacity
A
IRV + TV
16
Q
Functional Residual Capacity
A
RV + ERV (volume in lungs after normal expiration)
17
Q
Vital Capacity (VC)
A
TV + IRV + ERV
-maximum volume of gas that can be expired after a maximal inspiration
18
Q
Total Lung Capacity
A
= IRV + TV + ERV + RV
-volume of gas present in lungs after a maximal inspiration
19
Q
Determination of physiologic dead space
A
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
20
Q
Lung & Chest Wall
A
- 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
21
Q
Hemaglobin
A
- 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
22
Q
Hemoglobin Modifications
A
Lead to tissue hypoxia from dec. O2 saturation and dec. O2 content
23
Q
Methemoglobin
A
- 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+
24
Q
Carboxyhemoglobin
A
- 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
25
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.
26
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)
27
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
28
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
29
Primary Pulmonary HTN
-due to an inactivating mutation in the BMPR2 gene (normally functions to inhibit vascular smooth muscle proliferation); poor prognosis
30
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)
31
Pulmonary Vascular Resistance
PVR = P (pulmonary artery) - P (L atrium) / cardiac output
change in P = Q X R
R = 8nl/pir^4
32
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
33
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)
```
34
Hypoxemia
dec. PaO2
- normal A-a gradient (high altitude, hypoventilation)
- inc. A-a gradient (V/Q mismatch, diffusion limitation, right-to-left shunt)
35
Hypoxia
dec. O2 delivery to tissue
- dec. cardiac output
- hypoxemia
- anemia
- CO poisoning
36
Ischemia
loss of blood flow
- impeded arterial flow
- reduced venous drainage
37
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
38
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
39
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
40
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
41
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
42
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
43
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
44
Emphysema
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
45
Asthma
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
46
Bronchiectasis
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
47
Restrictive Lung Disease
-restricted lung expansion causes dec. lung volumes (dec. FVC and TLC)
-PFTs - FEV1/FVC ratio > 80%
Types:
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)
48
Pneumoconioses
-anthracosis, silicosis, & asbestosis, inc. risk of cor pulmonale & Caplan's syndrome
49
Anthracosis
Pneumoconioses
- associated with coal mines "coal miner's lung"
- affects upper lobe
50
Silicosis
Pneumoconioses
- 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
51
Asbestosis
Pneumoconioses
- 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
52
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
53
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
54
Obstructive vs. Restrictive Lung Disease
normal FEV1/FVC = 80%
obstructive FEV1/FVC < 80%
restrictive FEV1/FVC > 80%
55
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
56
Lung Physical Findings: Pleural Effusion
Breath sounds: dec.
Percussion: Dull
Fremitus: dec.
Tracheal Deviation: none
57
Lung Physical Findings: Atelectasis
```
bronchial obstruction
Breath sounds: dec.
Percussion: Dull
Fremitus: dec.
Tracheal Deviation: toward side of lesion
```
58
Lung Physical Findings: Spontaneous Pneumothorax
Breath sounds: dec.
Percussion: hyperresonant
Fremitus: dec.
Tracheal Deviation: toward side of lesion
59
Lung Physical Findings: Tension Pneumothorax
Breath sounds: dec.
Percussion: hyperresonant
Fremitus: dec.
Tracheal Deviation: away from lesion
60
Lung Physical Findings: Consolidation
```
(lobular pneumonia, pulmonary edema)
Breath sounds: bronchial breath sounds; late inspiratory crackles
Percussion: Dull
Fremitus: inc
Tracheal Deviation: none
```
61
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
62
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
63
Lung Cancer: Squamous Cell Carcinoma
Location: central
- hilar mass arising from bronchus: Cavitation; Cigarettes; hyperCalcemia (produces PTHrP)
- Keratin pearls & intercellular bridges
64
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
65
Lung Cancer: Large Cell Carcinoma
Location: Peripheral
- highly anaplastic undifferentiated tumor; poor prognosis
- less responsive to chemo, removed surgically
- pleomorphic giant cells
66
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 +
67
Lung Cancer: Mesothelioma
Location: pleural
- Malignancy of the pleura associated with asbestosis
- Results in hemorrhagic pleural effusions & pleural thickening
- Psammoma bodies
68
Pancoast Tumor
-Carcinoma that occurs in apex of lung may affect cervical sympathetic plexus, causing Horner's Syndrome
69
Horner's Syndrome
-ipsilateral ptosis, miosis, anhidrosis
70
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
71
Lobular Pneumonia
S. pneumoniae most frequently, Klebsiella
| -intra-alveolar exudate - consolidation; may involve entire lung
72
Bronchopneumonia Pneumonia
S. pneumoniae, S. aureus, H. influenzae, Klebsiella
| -Acute inflammatory infiltrates from bronchioles into adjacent alveoli; patchy distribution involving > 1 lobe
73
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
74
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)
75
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
76
Pleural Effusions: Transudate
- dec. protein content
| - due to CHF, nephrotic syndrome, or hepatic cirrhosis
77
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
78
Pleural Effusions: Lymphatic
- also known as chylothorax
- due to thoracic duct injury from trauma, malignancy
- milky-appearing fluid, inc. triglycerides
79
Pneumothorax
unilateral chest pain & dyspnea, unilateral chest expansion, dec. tactile fremitus, hyperresonance, diminished breath sounds
80
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
81
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
