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65 Cards in this Set
- Front
- Back
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mechanical properties of the lung
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static: no airflow
dynamic: during airflow |
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static passive forces
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lung elastic recoil: elastin within the lung parenchyma
coupling b/w lung & chest wall - pleural fluid couples lung to chest wall ; establishes functional residual capacity: FRC - thoracic cage holds lungs at FRC; introducing air into pleural space causes lung to collapse =pneumothorax: air in pleural space |
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static measurement
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compliance: distensibility of lung
defined by slope of pressure: volume curve during a breath how much P does it take to provide the tidal volume |
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dynamic active forces
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muscle work
- inspriation: diaphragm, external intercostals, sternocleidomastoid -expiration: passive process except durinig exercise; abdominal muscles (rectus, internal & external obliques, transversus abdominus) and internal intercostals airway resistance: - turbulence: mostly in upper airawys - resistance to laminar flow highest in terminal bronchioles dynamic compression of airways - clinically important during forces expiration |
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lung mechanics
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pulmonary function testing
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pulmonary function testing includes
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spirometry
lung volumes diffusion capacity |
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spirometry
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used to directly measure tidal vol, inspiratory reserve volume, and expiratory reserve volume
sume of which is vital capacit take big breath and blast out as quickly as can |
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lung volumes in pulmonary function testing
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4 methods
- plethysmography, HE dilution, N2 washout and chest imaging measures VC and total lung capacity - residual vol calculated TLC-VC = RV |
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diffusion capacity in PFT
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single breath with 0.3% CO
transfer factor can't directly measure RV so measuure how much CO comes back when exhale; if taken u well, less CO comes back |
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obstruction
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lungs: more compliant in emphysema, not all
airways: increased R in asthma, bronchitis spirometry: FEV1/FVC : low lung volumes: TLC & RV increased diffusing capacity decreased Ex: COPD, CF, Asthma |
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restriction
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lungs: stiff ; not always due to fibrosis (pulmonary edema and other infiltrates)
airways usually normal spirometry - FEV1/FVC - normal to high (b/c both suppressed) - FEV1 and FVC low lung volumes: TLC decreased diffusing capacity decreased Ex: ARDS - atelectasis, fibrotic lung dz, kyphoscoliosis causes chest wall restriction |
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PFTs in COPD
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functional changes include:
increased - TLC - FRC - RV unchanged - ERV & Vt decreased - IRV & IC |
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spirometry measures
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flow volume loop
measures FEV1 |
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ventilation definitions
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minute ventilation
alveolar ventilation anatomic dead space physiologic dead space dead space ventilation |
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minute ventilation
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Vt x f
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alveolar ventilation
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(Vt-Vd) x f
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anatomic dead space
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volume estimated by ideal body wt in lbs
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physiologic dead space
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Vd/Vt = PaCO - PetCO / PaCO
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dead space ventilation
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wasted ventilation decreases with exercise
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regional distribution of ventilation
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gravity pulls lung mass down
less dependent alveoli are more distended dependent alveoli are more compliant - can distend more, accept more of inspired air effect is less pronounced in supine position diseasae creates regional variations in ventilation |
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closing volume
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single breath N2 washout
rarely used clinically |
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pulmonary circulation
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low resistance circuit
- shorter, no precapillary sphincters, parallel circuit - Pressures measured clinically in mmHg (pulmonary A) if higher than 15-30 =pulmonary HTN |
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regional distribution of blood flow in pulmonary circulation
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zones defined by arterial (Pa), venous (Pv) and alveolar Pressures (PA)
zones 1-4 |
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zone 1
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alveolar P > arterial P > venous P
- no blood flow dead space ventilation alveolar pressure collapses BV; not good gas exchange |
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zone 2
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arterial P > alveolar P > venous P
less blood flow but zones 2,3 are best gas exchange b/c alveoli open and art P pushes past alveolar P |
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zone 3
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pulmonary A & V P > alveolar P
veins distended gravity effects flow |
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zone 4
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base of lung
area of decreased blood flow |
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regulation of resistance
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passive & active
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passive regulation of resistance
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recruitment: increased PASP converts zone 1 to 2 (exercise)
distention: expansion of inflated lung pulls pulmonary caps open |
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active regulation of resistance
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hypoxic pulmonary vasoconstriction
vascular endothelial mediators |
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hypoxic pulmonary vasoconstiction in active resistance
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decrease PO2 in alveoli causes local arterial vasoconstriction
diverts perfusion away from poorly ventilated areas to better ventilated alveoli |
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vascular endothelial mediators in active R
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endothelin 1
prostacyclin NO: constituently produces; keeps A's open |
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fluid exchange
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starling forces
pulmonary edema/pleural effusions shunts disorders |
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starling forces
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helps ID pathologic mechanism in pleural effusion
Jv = Kf [(P cap - P int) - (P cap - P int)] |
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pulmonary edema/pleura effusions example
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HR
increase P cap; pulmonary edema renal/liver dz decrease P cap: fluid leaks out cap to alveolar and pleural space |
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shunts
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anatomic abnormality allowing blood to bypass gass exchange areas
- patent ductus arterioisis & VSD venous admixture: mixing of oxygenated & deoxygenated blood - coellesce when go back to L atrium |
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disorders in fluid exchange
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pulmonary HTN
pulmonary embolism pulmonary vasculitis |
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gas exchange depends on
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diffusion: dependent on area, thickness, soluability, pressure
gas transfer (DLCO2) - measured using CO as it avidly binds to Hgb - DCO is 20x greater than DLO2 so its perfusion is limited - O2 is usually perfusion limited but can become diffusion limited in disease states |
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alveolar gas equations
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CO2
- PCO is dependent on ventilation & metabolism O2 *** - PAO2 = (FiO2)(patm-PH20) - PaCO2/RQ - respiratory quotient = VCO2/VO2 = about 0.8 alveolar-arterial gradient - PaO2 and PaCO2 measured - calculate PAO2 |
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A-a gradient
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PAO2-PaO2
normal =age/4 measure of efficiency of oxygenation lower # = less efficeint oxygenation is |
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V/Q inequality
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spectrum of V/Q
approaching zero - shunts - airway obstuction, pulm edema, atelectasis - little ventilation, large flow approaching infinity - alveolar dead space - pulm embolism, MI (RV) - not good gas exchange/vent |
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hypoxia
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decreased partial P of O2 in inspired air or content of O2 in tissues
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hypoxemia
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decreased partial P of O2 in blood
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5 causes of hypoxemia via lungs
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hypoxia
diffusion block V/Q mismatch hypoventilation shunt (decreased O2 delivery) supplemental O2 does not reverse hypoxemia of shunt |
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control of ventilation
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controllers in pons/medulla
chemoreceptors pulmonary receptors fever, increase progersterone increase respiratory rate |
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chemoR's in control of ventilation
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central: sens to PaCO
increases depth of inspiration peripheral : sens to paCO, PaO increases rate & depth of inspiration |
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pulmonary R's in control of ventilation
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stretch R's : inhibit overdistention
irritant R's : cough J R's (C fibers): cause burning sensation |
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dyspnea
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awareness of breathing
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tachypnea
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increase resp rate
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kussmaul's
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increased tidal vol
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biot's
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periodic or cluster breathing
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Cheyn-stokes
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stairstep, waxing/waning
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apnea
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central: congenital, neuromuscular
obstructive: upper airway obstruction |
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special environments
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high altitude: hypoxemia cuased by low P O2; hyperventilation is first response
oxygen toxicity fetal gas exchange diving medicine: P increases by 1 atm for every 33 ft - descent can cause TM rupture, "squeeze" - ascent can cause "bends" : gas comes out of solution too quickly, pneumothroax; hyperbaric tx needed for bends |
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airways
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nasal passages
- alpha agonists constrict nasal vasculature - anti choliinergics block mucus production trachea & large airways - muco-ciliary escalator; major role in lung defense - methacholine challenge may be positive in allergic rhinits & asthma |
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respiratory defense
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resp airay cells: sme in upper & lower airways
inflammation - mast cells: release multiple pro-inflammatory meditors - neutrophils: release elastases, proteases,produce O2 radicals - eosinophils: more prevalent in allergy/asthma |
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acid base balance
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1 of 3 physiological methods
lungs play role, kidney more effective |
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respiratory acidosis
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PaCO elevatted
pH low chronic: PaCO2 elevated, pH normal, bicarb elevated acute on chronic: same as above, but pH low |
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resp alkalosis
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PaCO decreased
pH elevated can occur if chronic resp acidosis is hyperventilating |
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reading a chest radiograph
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be consistent, follow same pattern
review pt detials & history, orientation, rotation, adequacy of inspiration, penetration, exposure |
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mnemonic approach to reading CXR
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Airways
bones cardiac diaphragm effusions/extrathoracic fields gastric bubble |
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structural appraoch to reading CXR
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look for opacities
check mediastinal contours check cardio thoracic ratio check heart borders check hilar structures check lung fields diaphragm contours bones |
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diaphragm should be b/w what ribs on CxR
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9/10 in midclavicular line
if not = atelectasis if 11-12: hyperinflation |
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CT mediastinal views
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used to examin LN's and vasculature (if contrast used)
- LN's numbered from top to bottom - used to stage lung cancer |
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summary
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acid base: physiologic method used in this core
Chest imaging - chest radiographs; use consistent pattern for reding - chest computed tomography: lung & mediatinal (at clavicles) windows |
