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35 Cards in this Set
- Front
- Back
Central chemoreceptors
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Medulla
Directly sense decreasing pH (increasing H+) Stimulated by PCO2 via BBB diffusion and formation of H+ * COPD pts w/ chronic hypercapnia: high [CO2] stops stimulating respiratory center - hypoxia remains only remaining drive, so if supplemental O2 is admin this is dangerous because then the stimulus disappears and respiration is inhibited --> respiratory failure |
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Peripheral chemoreceptors
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Carotid/aortic bodies
Respond to hypoxia (senses PaO2) |
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Right lobe aspiration
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Right side because right main stem bronchus more vertical and wider than left
If aspirate while upright = inferior portion of inferior lobe If aspirate while supine = superior portion of inferior lobe |
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Pulmonary artery and bronchus
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RALS
Right, Anterior Left, Superior |
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Diaphragm structures
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Perforating diaphragm
T8 = IVC T10 = esophagus, vagus (2 trunks) T12 = aorta, thoracic duct, azygous vein Diaphragm innervation: C3-5 = phrenic N. Referred pain = shoulder and neck |
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Pulmonary vessel anatomical relationships
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Pulmonary trunk = unox blood
- conus arteriosus from RV - at sternal angle --> R+L pulmonary arteries (most superior vessels in hilum of each lung) Right pulmonary artery - passes laterally - posterior to asc. aorta & SVC - to R hilum of R lung Left pulmonary artery - anterior to descending thor. aorta - to L hilum of L lung Pulmonary veins = ox. blood - 2 pulm v. / lung exit hilum anteriorly & inferiorly pulm arteries - 4 pulm veins drain into the LA |
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Thoracocentesis
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Miclavicular line = 5-7 ribs
Midaxillary line = 7-9 ribs Paravertebral line = 9-11 ribs |
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Exercise: Muscles of respiration
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Inspiration = external intercostals, scalenes, sternomastoids
Expiration = rectus abdominis, internal/external obliques, transversus abdominis, internal intercostals |
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Angiotensin converting enzyme (ACE)
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AngioI --> Angio II cnversion
Inactivates bradykinin (ACE-I's increase bradykinin and cause cough, angioedema) Kallikrein - activates bradykinin |
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Capacity
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sum of >2 volumes
Vital capacity = TV + IRV + ERV FRC = RV + ERV * lowest PVR IC = IRV + TV TLC = IRV + TV + ERV + RV |
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Ventilation
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Minute ventilation = includes all air
Tidal vol x (breaths/min) Alveolar ventilation = refers ONLY to air participating in gas exchg/min Tidal vol - dead space x (breaths/min) Dead space = vol of air that does NOT participate in gas exchg; apex of lung contributes most to this Vd = Vt x (PaCO2- PeCO2)/PaCO2 |
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Hb modifications
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TISSUE HYPOXIA (from dec O2 sat)
Methemoglobin: - Nitrite drugs cause Fe2+ (normal iron in Hb)-->Fe3+ - Fe3+ Hb does not bind O2 as readily but has inc affinity for CN- - CN- also inhibit cyto c oxidase (but preferentially bonds to MetHb instead) * Note: partial P of O2 in blood remains NORMAL b/c amt of dissolved O2 in plasma = same (O2's partial P is not related to Hb fxn) - Tx: Thiosulfate binds CN- --> thiocyanate (renally excreted) or tx w/ methylene blue CarboxyHb: - CO bound instead of O2 to Hb - Dec O2 binding --> Lshift on curve - Dec O2 tissue unloading |
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O2-Hb dissociation curve
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Right-shift = decreased Hb affinity for O2 = O2 tissue unloading caused by an increase in ALL factors:
- dec O2 affinity, inc P50 - inc metabolic needs - inc PCO2 - inc temp - inc H+/dec pH - high altitude, inc 2,3,-DPG Left-shift: a decrease in ALL factors: - inc Hb-O2 affinity, dec P50 - dec met needs - dec PCO2, dec temp - dec H+/inc pH - dec 2,3,-DPG - Fetal Hb!!! P50 = partial P of O2 in blood at which Hb is 50% sat (26mmHg is nl) |
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Perfusion limited
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Rapidity with which alveolar air equilibrates with partial P of O2 + CO2 in blood depends on how quickly a given vol. of blood can course through alveolar capillaries
CO2, N2O Gas equilibrates early along length of capillary Diffusion can be increased only if blood flow increases |
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Diffusion limited
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O2 (emphysema, fibrosis), CO
Gas does not equilibrate by time blood reaches end of capillary |
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Pulm HTN
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Nl pulm artery pressure = 10-14mmHg
Pulm HTN = >25 mmHg or >35 mmHg during exercise S2 split present If 1* - due to inactiv mut in BMPR2 that normally functions to inhibit vascular smooth muscle proliferation; requires lung transplant |
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PVR
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PVR = [P(pulm artery) - P(Latrium)]/CO
R = 8nl/pie(r^4) * major site of airway R = med-sized bronchi (>2mm) * small airways do not contribute to R as much b/c of PARALLEL arrangement Parasymp stim = inc R Symp stim = dec R |
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Total O2 content
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Affected by 3 main variables:
1. [Hb] 2. O2 saturation of Hb 3. Partial P of O2 dissolved in blood |
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A-a gradient
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PAO2 - PaO2 = 10-15 (nl)
PAO2 = 150 - PACO2/0.8 Helps determine cause of hypoxemia |
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Hypoxemia
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Dec PaO2
If normal A-a grad: 1. High altitude 2. Hypoventilation If inc A-a grad: 1. V/Q mismatch 2. Diffusion limitation 3. R-L shunt |
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Hypoxia
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Dec O2 deliv to tissues
1. Dec CO 2. Hypoxemia 3. Anemia 4. CN poisoning 5. CO poisoning |
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Ischemia
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Loss of blood flow
1. Impeded arterial flow 2. Reduced venous drainage |
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CO2 transport
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CO2 transported from tissues --> lungs in 3 forms:
1. Bicarbonate (transported in blood) = 90% 2. CarbaminoHb (bound to Hb) = 5% 3. Dissolved CO2 (5%) |
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Sleep apnea
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Central (no resp effort) v. Obstructive (resp effort)
Peritubular cells in renal cortex sense hypoxia and respond by releasing EPO --> 2* polycythemia |
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Physical lung findings: bronchial obstruction
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- absent/dec breath sounds over area
- dec resonance - dec fremitus - trach deviation TOWARDS sign of lesion |
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Pleural effusion
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- dec breath sounds over effusion
- dull resonance - dec fremitus |
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Pneumonia
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- bronchial breath sounds over lesion
- dull resonance - inc fremitus |
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Tension pneumothorax
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dec breath sounds
hyperresonance absent fremitus trach dev AWAY from side of lesion |
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Lung CA complications
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Pancoast tumor
- may affect cervical symp plexus --> Horner's syndrome (ptosis, miosis, anhidrosis) - can invade brachial plexus --> weakness/paresthesias of arm SVC syndrome - SVC has thin walls so easily compressible by mediastinal masses - usu assoc w/ bronchogenic CA or NHL - sx's include dyspnea, cough, facial swelling, UE/ncek swelling, tracheal compromise |
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Squamous Cell Carcinoma
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Hilar mass central, from bronchys
Cavitation Smoking associated PTHrP --> hypercalcemia Keratin pearls and intracellular bridges |
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Small cell Carcinoma
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Central location
ACTH/ADH production LE syndrome NE cells w/ granules |
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Lobar Pneumonia
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4 stages
1. Congestion - 1st 24h - red heavy boggy w/ vascular dilation, alveolar exudate w/ bacteria 2. Red hepatization -2-3d; red firm lobe - alveolar exudate 2/ erythrocytes, neutrophils, fibrin 3. Gray hepatization - 4-6d - gray brown firm lobe w/ RBCs disintegrated, alevolar exudate contains neutrophils + fibrin 4. Resolution - restoration of normal architecture - enzymatic dig of exudate |
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Pulmonary alveolar proteinosis
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autoAbs against GM-CSF
impaired surfactant CL by alveolar macrophages |
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Chylothorax
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Disruption of thoracic duct in posterior chest via malignant neoplasms (NH lymphoma)
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Farmer's Lung
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= hypersensitivity pneumonitis
Type III/IV reaction (Type IV only when chronic exposure to Ag) Granulomas can form but dz abates when Ag exposure stops |