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Respiratory - Anatomy & Physiology

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welejofo's version from 2017-04-28 19:35

Anatomy

Question Answer
What extends only to the end of the bronchi?Cartilage, goblet cells
Type 1 pneumocytes97% of alveolar surfaces
Line the alveoli
Squamous (thin) for optimal gas exchange
Type 2 pneumocytesSecrete pulmonary surfactant → ↓ alveolar surface tension and prevention of alveolar collapse (atelectasis
Cuboidal, clustered
Precursors for type 1 cells and type 2 cells - proliferate during lung damage
Clara cellsNon-ciliated
columnar with secretory granules that secrete surfactant component
Degrade toxins
Act as reserve cells
Collapsing pressure =2(surface tension)/radius
Lecithinsmake up pulmonary surfactant
Most important part of surfactant (lecithins)dipalmitoylphosphatiydulcholine
Surfactant synthesis - when it begins, endsBegins week 26
Lungs are mature around week 35 when lecithin:sphingomyelin ration is > 2 in the amniotic fluid.
Left lung has how many lobes?2 + lingula
Right lung has how many lobes?3
Aspirate location if done while uprightlower portion of right inferior lobe
Aspirate location if done while supinesuperior portion of right inferior lobe
What perforates the diaphragm at T8?IVC
What perforates the diaphragm at T10esophagus, vagus (2 trunks)
What perforates the diaphragm at T12aorta, thoracic duct, azygos vein
Diaphragm innervated byC3,4,5
Accessory muscles for inspiration while exercisingexternal intercostals, scalene muscles, sternocleidomastoids
Accessory muscles for expiration while exhalingrectus abdominis, internal and external obliques, transversus abdominis, internal intercostals
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Lung volumes

Question Answer
Inspiratory reserve volumeair that can still be breathed in after normal inspiration
Tidal volumeair that moves into lung with each quiet inspiration, typically 500 mL
Expiratory reserve volumeAir that can still be breathed out after normal expiration
Residual volumeair in lung after maximal expiration
cannot be measured on spirometry
Inspiratory capacityIRV + TV
Functional residual capacityRV + ERV
volume in lungs after normal expiration
Vital capacityTV + IRV + ERV
maximum volume of gas that can be expired after maximal inspiration
Total lung capacityIRV + TV + ERV + RV
Volume of gas present in lungs after a maximal inspiration
Equation to determine physiologic dead spaceVD = TV x (PaCO2 - PECO2)/PaCO2
Taco, Paco, PEco, Paco
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More physiology

Question Answer
The best way to think about pulmonary complianceit's the opposite of elasticity
Diseases/conditions that decrease compliancepulmonary fibrosis, pneumonia, pulmonary edema
Diseases/conditions that increase complianceemphysema, normal aging
Hb T form (taut) affinity for O2low affinity for O2
Hb R (relaxed form) affinity for O2high affinity for O2
What shifts O2-Hb curve to the left?a ↓ in all factors (except pH)
left shift = ↑ affinity of Hb for O2
What shifts O2-Hb curve to the right?a ↑ in all factors (except pH)
think: The O2/Hb curve is upright
up the O2 in it's rightful place (the tissues)
right shift = ↓ affinity of Hb for O2
Affinity after 1,2,or3 O2 units bind to HbAffinity for O2 increases for each subsequent O2 molecule
↓ in PAO2 causeshypoxic vasoconstriction → shifts blood away from poorly ventilated areas
Perfusion limited gasesO2 (in normal, healthy pts), CO2, N2O
gas equilibrates early along the length of the capillary
to ↑ diffusion you must ↑ blood flow
Diffusion limited gasesO2 (in emphysema(↓ Area), fibrosis(↑ Thickness)), CO
Gas does not equilibrate by the time it reaches the end of the capillary
Diffusion of gas equationV(gas) = A/T x D(P1-P2)
Cause of 1° pulmonary hypertensioninactivating mutation in the BMPR2 gene (it normally inhibits vascular smooth muscle proliferation)
poor prognosis
Causes of 2° pulmonary hypertensionCOPD
mitral stenosis
recurrent thromboemboli
autoimmune disease
left-to-right shunt
sleep apnea
living at high altitude
Course of pulmonary hypertensionsevere respiratory distress → cyanosis and RVH → death from decompensated cor pulmonale
How does it cause pulmonary hypertension?: COPDdestruction of lung parenchyma
How does it cause pulmonary hypertension?: Mitral stenosis↑ resistance → ↑ pressure
How does it cause pulmonary hypertension?: Recurrent thromboemboli↓ cross-sectional area of pulm vascular bed
How does it cause pulmonary hypertension?: Autoimmune diseasesystemic sclerosis; inflammation → intimal fibrosis → medial hypertrophy
How does it cause pulmonary hypertension?: Left→right shunt↑ shear stress → endothelial injury
How does it cause pulmonary hypertension?: sleep apnea or living at high altitudehypoxic vasoconstriction
Pulmonary vascular resistance equation: PVR =(Ppulm artery - PL atrium)/cardiac output
ΔP =Q x R
R =8ηl/πr^4
η= the viscosity of blood; l=vessel length; r=vessel radius
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Oxygen content and more physio

Question Answer
O2 content of blood =(O2 binding capacity x %sat) + dissolved O2
Normally 1g Hb can bind to how much O2?1.34 mL O2
Normal amount of Hb in blood15 g/dL
Cyanoiss results when deoxygenated Hb is....> 5 g/dL
O2 binding capacity =20.1 mL O2/dL
What O2 measurements fall and don't fall when Hb falls?O2 content of arterial blood falls
O2 sat and arterial PO2 don't fall
Oxygen delivery to tissues =cardiac output x O2 content of blood
Alveolar gas equationPAO2 = PIO2 - (PaCO2/R)
PAO2=alveolar PO2
PIO2 = PO2 in inspired air
PaCO2 = arterial PCO2
R = respiratory quotient = CO2 produced/O2 consumed
Approximation of alveolar gas equationPAO2 = 150-PaCO2/0.8
Normal A-a gradientPAO2-PaO2 = 10-15 mmHg
↑ in hypoxemia
causes of ↑: shunting, V/q mismatch, fibrosis (impairs diffusion)
Hypoxemia (↓ PaO2) with a normal A-a gradienthigh altitude
hypoventilation
Hypoxemia (↓ PaO2) with an ↑ A-a gradientV/Q mismatch
Diffusion limitation
R→L shunt
Hypoxia (↓ O2 delivery to tissue)↓ cardiac output
hypoxemia
CO poisoning
Ischemia (loss of blood flow)Impeded arterial flow
reduced venous drainage
V/Q = 3 means....Wasted ventilation
apex of the lung
V/Q = 0.6 means....Wasted perfusion - less ventilation
base of the lung
V/Q in a shunt situation=0
100% O2 does not improve PO2
V/Q in an obstruction (thromboembolus)→infiniti
physiologic dead space
100% O2 improves PO2
CO2 equilibrium equationCO2 + H20 ↔ H2CO3 ↔ H + HCO3
Haldane effectOxygenation of Hb → dissociation of H from Hb → shifts CO2 eq. towards CO2 formation → CO2 is released from RBCs
In the lungs
Bohr effect↑ H from tissue metabolism shifts curve to the right, unloading O2
in peripheral tissue
Effects of high altitude↑ ventilation
↑ erythropoietin → ↑ hematocrit and Hb
↑ 2,3-BPG - binds to Hb so that Hb releases more O2
↑ mitochondria
↑ renal excretion of bicarb - take acetazolamide to compensate for the respiratory alkalosis
Chronic hypoxic pulm vasoconstriction → RVH
Response to exercise↑ CO2 production
↑ O2 consumption
↑ ventilation rate to meet O2 demand
V/Q ratio from apex to base becomes more uniform
↑ pulmonary blood flow d/t ↑cardiac output
↓ pH during strenuous exercise (2° to lactic acidosis)
No change in PaO2 and PaCO2, but an ↑ in venous CO2 content and ↓ in venous O2 content
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