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30 Cards in this Set
- Front
- Back
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What indicates fetal lung maturity?
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lecithin-to-sphingomyelin ratio of > 2.0 in amniotic fluid
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Type II pneumocytes
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secrete pulmonary surfactant (dipalmitoyl phophatidylcholine)
precursors to type I cells (proliferate during lung damage) & other type II |
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Inhaled foreign body goes where?
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right lung b/c right main bronchus is wider & more verticle
while upright --> lower portion of right inferior lobe while supine --> superior portion of right inferior lobe |
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Relation of pulmonary artery to bronchus at each lung hilus?
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RALS
right anterior left superior |
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MM respiration
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Inspiration
**external intercostals (pulling air from the external environment) **scalene mm **sternomastoids Expiration **rectus abdominus **internal & external obliques **transversus abdominis **internal intercostals |
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Kallikrein
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Kallikrein is produced by the lung
activates bradykinin ACE inactivates bradykinin (cough, angioedema w/ACE inhibitors) |
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Collapsing pressure of lung
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Collapsing pressure of lung
P = 2 (surface tension) / radius **tendency to collapse increases on expiration with decreasing radius |
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Lung Volumes
Residual Volume (RV) Expiratory reserve volume (ERV) Tidal volume (TV) Inspiratory reserve volume (IRV) Vital capacity (VC) Functional residual capacity (FRC) Inspiratory capacity (IC) Total lung capacity (TLC) |
Lung Volumes:
**see page 561 (585 in pdf) Vital capacity is everything but the residual volume. A capacity is a sum of >= 2 volumes. 1. Residual volume ( RV) -air in lung after maximal expiration; cannot be measured on spirometry 2. Expiratory reserve volume (ERV) -air that can still be breathed out after normal expiration 3. Tidal volume (TV) -air that moves into lung with each quiet inspiration, typically 500 mL 4. Inspiratory reserve volume (IRV) -air in excess of tidal volume that moves into lung on maximum inspiration 5. Vital capacity (VC): TV + IRV + ERV 6. Functional residual capacity (FRC ) : RV + ERV (volume in lungs after normal expiration) 7. Inspiratory capacity (IC ) : I RV + TV 8. Total lung capacity: TLC = I RV + TV + ERV + RV |
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Physiologic Dead Space
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Physiologic Dead Space = anatomical dead space + fxnl dead space (apex of healthy lung is biggest contributor)
Vd = Vtidal * [ PaCO2 - Pexpired CO2 ] / PaCO2 **conceptually, if all the CO2 in arteriole were exchanged then Vd = 0. This measures the fraction that is not exchanged. |
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Lung & Chest Wall
-balance pt? -compliance? |
Lung & Chest Wall
-balance pt? **inward pull lungs balances outward pull chest wall at FRC **airway & alveolar pressure 0; pleural pressure negative -compliance? ** C = change in Volume / change in pressure **decreased compliance with: ***pulmonary fibrosis ***insufficient surfactant ***pulmonary edema |
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Hemoglobin
-2 forms -shifts |
Hemoglobin
-2 forms **T (taut) form has low O2 affinity **R (relaxed form) has 300x O2 affinity -shifts **RIGHT SHIFT - favors T, O2 dissociation ***Cl- ***[H] (lower pH) ***CO2 ***2,3-BPG ***temperature **LEFT SHIFT - favors R, O2 bound more tightly ***Fetal Hemoglobin (2 alpha 2 gamma) - lower affinity for 2,3-BPG, higher affinity O2 When you're Relaxed you're doing things Right - carrying O2 |
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Methemoglobin
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Methemoglobin
Oxidized form (Fe3+) Does not bind O2 well METHemoglobinemia tx w/METHylene blue has increased affinity for CN- tx CYANIDE POISONING by using NITRITES to oxidize Hb which binds up CN-; THISULFATES bind this cyanide --> thiocyanate, renally excreted |
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Carboxyhemoglobin
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Carboxyhemoglobin
CO binds hemoglobin (200x > affinity than O2) Decreased O2 carrying capacity Left shift --> decreased O2 unloading **CO does increase Hb saturation at any given PO2 b/c of positive cooperativity |
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Right shift in Hb-O2 curve
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Right shift in Hb-O2 curve
C-BEAT CO2 2,3-BPG Exercise Acid/Altitude Temperature |
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Pulmonary Circulation
-perfusion limited -diffusion limited |
Pulmonary Circulation
-perfusion limited **gas (O2, CO2, N2O) equilibrates early along length of capillary **diffusion can only be increased by increasing blood flow -diffusion limited **O2 (emphysema & fibrosis), CO **gas does not equilibrate by time blood reaches end of capillary Diffusion: Vgas = Area / thickness x Dk (P1 - P2) -Area decreases in Emphysema -Thickness increases in pulmonary fibrosis |
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Pa vs PA
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PA = partial pressure in alveolar air
Pa = partial pressure in pulmonary capillary blood |
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Pulmonary Hypertension
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Pulmonary Hypertension
normal pulm. artery pressure = 10-14 mmHg pulm HTN = >25 mmHg (or >35 mmHg in exercise) Results in: **atherosclerosis **medial hypertrophy **intimal fibrosis of pulmonary arteries Course: severe respiratory distress --> cyanosis & RVH --> death from decomponsated cor pulmonale |
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Pulmonary Hypertension: Primary Causes
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Pulmonary Hypertension: Primary Causes
**inactivating mutationin BMPR2 **normally inhibits vascular smooth muscle proliferation **poor prognosis |
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Pulmonary Hypertension: Secondary Causes
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Pulmonary Hypertension: Secondary Causes
**COPD - destruction of lung parenchyma **mitral stenosis - increased pressure **recurrent thromboemboli - decreased cross-sectional area of pulm. vascular bed **autoimmune disease - inflammation - intimal fibrosis - medial hypertrophy (ie systemic sclerosis) **sleep apnea / high altitude - hypoxic vasoconstriction |
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Pulmonary Vascular Resistance (PVR)
[calculation] |
Pulmonary Vascular Resistance (PVR)
PVR = [Ppulm artery - Pleft atrium] / cardiac output **V = IR; V=pressure gradient; I = output R = 8*n*l / (pi * r^4) **n = blood viscosity **l = length of vessel **r = radius of vessel |
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Oxygen Content of Blood
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Oxygen Content of Blood
O2 content = [O2 binding capacity x % saturation] + dissolved O2 **O2 binding capacity nl ~20.1 mL O2/dL **nl 1 g Hb binds 1.34 mL O2; nl Hb ~ 15 g/dL **cyanosis when deoxygenated Hb > 5 g/dL |
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Alveolar Gas Equation
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Alveolar Gas Equation
PAO2 = PIO2 - (PaCO2 / R) [R ~ 0.8] A-a gradient = 10-15 mmHg **increased with: hypoxemia - shunting, V/Q mismatch, fibrosis R = respiratory quotient = CO2 produced / O2 consumed |
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Causes of increased A-a gradient
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Causes of increased A-a gradient
*nl = 10-15 mmHg Hypoxemia **shunting (R-->L) **V/Q mismatch **Diffusion limitation (pulmonary fibrosis) |
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Causes of Hypoxemia w/nl A-a gradient
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Causes of Hypoxemia w/nl A-a gradient
high altitude hypoventilation |
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Causes of hypoxia
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Causes of hypoxia
Hypoxia = decreased O2 delivery to tissue **decreased cardiac output **hypoxemia (decreased PaO2) **anemia **cyanide poisoning **CO poisoning |
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V/Q mismatch
*nl phys *lung zones *path states |
V/Q mismatch
Normal Phys: *should be matched to ~1 *exercise (increased Card Output) causes vasodilation; V/Q approaches 1 Lung Zones: *apex: V/Q --> 3; wasted ventilation *base: V/Q --> 0.6; wasted perfusion Pathologic: V/Q --> 0; ventilation obstruction [shunt]; 100% O2 does not help PaO2 V/Q --> infinity; perfusion obstruction; 100% O2 does help PaO2 [assuming less than complete dead space] |
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Hypoxemia that
*responds to 100% FIO2 *does not respond to 100% FIO2 |
Hypoxemia that
*responds to 100% FIO2 --> blood flow obstruction (physiologic dead space) *does not respond to 100% FIO2 --> airway obstruction [shunt] **Assumes less than 100% dead space w/perfusion obstruction |
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CO2 Transport
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CO2 Transport
1.) as HCO3- (90%) 2.) bound to Hb [N-terminal; carbaminohemoglobin] (5%) 3.) as dissolved CO2 **in formation of H2O + CO2 --> HCO3- + H+, the H+ ion binds Hb for transport |
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Haldane Effect vs Bohr Effect
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Haldane Effect vs Bohr Effect
Haldane Effect **effect of O2 on CO2 **in lungs high O2 --> H+-Hb & CO2-Hb unloading **in tissue low O2 --> CO2 & H+ loading Bohr Effect **effect of CO2/H+ on O2-Hb **in tissue high CO2/H+ --> O2 unloading [Right Shift] **in lungs low CO2/H+ --> O2 loading |
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Pharm tx for high altitude?
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Acetezolamide (carbonic anhydrase inhibitor)
-increase renal excretion of bicarb (body does this naturally too to compensate for resp alkalosis) |
