What makes up the Conducting Zone?
Large airways: Nose, Pharynx, Trachea, Bronchi
Small airways: Bronchioles and Terminal Bronchioles
Key Terms
What makes up the Conducting Zone?
Large airways: Nose, Pharynx, Trachea, Bronchi
Small airways: Bronchioles and Terminal Bronchioles
Function of Conducting Zone
Warms and humidifies air but does not participate in gas exchange
Anatomical Dead Space
Cartilage extends until
Bronchi
Goblet cells extend until
End of Bronchi
Pseudostratified, ciliated, columnar cells extend until
What is the cilia’s function?
End of Terminal Bronchioles to beat mucus up and out of lung
Smooth muscle in airway wall extends until
terminal bronchioles
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| Term | Definition |
|---|---|
What makes up the Conducting Zone? | Large airways: Nose, Pharynx, Trachea, Bronchi Small airways: Bronchioles and Terminal Bronchioles |
Function of Conducting Zone | Warms and humidifies air but does not participate in gas exchange Anatomical Dead Space |
Cartilage extends until | Bronchi |
Goblet cells extend until | End of Bronchi |
Pseudostratified, ciliated, columnar cells extend until What is the cilia’s function? | End of Terminal Bronchioles to beat mucus up and out of lung |
Smooth muscle in airway wall extends until | terminal bronchioles |
What makes up the respiratory zone? | = Lung Parenchyma. Respiratory bronchioles, alveolar ducts and alveoli participates in gas exchange |
What kind of cells are in the Respiratory zone? | Cuboidal cells in respiratory bronchioles, then simple squamous cells up to alveoli |
Type I Pneumocytes Percentage of alveolar surface Kind of cell Function | 97% of alveolar surface. Squamous cells optimal for gas diffusion |
Type II Pneumocytes Kind of cell Function | Clustered cuboidal cells. Secrete surfactant and act as precursors |
Collapsing Pressure Formula | P = 2 (surface Tension) / Radius |
When are alveoli most likely to collapse? | On Expiration |
Function of surfactant | Decreased alveolar surface tension to prevent atelectasis |
Composition of surfactant | Complex mix of lecithins. The most important of which is dipalmitoylphasphatidylcholine |
When does surfactant production begin in the fetus? When does it reach mature levels? What indicates maturity? | Begins at week 26. Mature by week 35. Mature when Lecithin/Sphingomyelin > 2 |
Clara Cells: Location Appearance Function | In Terminal and Respiratory Bronchioles. Non ciliated columnar cells with secretory granules. Secrete components of surfactant, degrade toxins and act as reserve cells |
of lobes in each lung? | R: 3, L: 2 + Lingula |
Foreign body most likely to be lodged in | R lung because R mainstem bronchus is wider and more vertical than L |
Aspirate a peanut: While upright? While supine? | Upright: Lower Portion of R Inferior Lobe Supine: Superior Portion of R Inferior Lobe |
Relationship bet Pul Artery to the Bronchus? | RALS Right: Anterior, Left Superior |
Structures perforating the Diaphragm | I ate 10 eggs at 12 T8: IVC T10: Vagus and Esophagus T12: Aorta, Azygous, Thoracic duct (Red White and Blue) |
What innervates the Diaphragm? Where is pain from the Diaphragm referred? | C3, 4, 5 keeps you alive Pain referred to shoulder (C5) and Trapezius ridge (C3, C4) |
Muscles of respiration (quiet and exercise) | Inspiration: Quiet –> Diaphragm, Exercise –> SCM, Scalene, External Intercostals Expiration: Quiet –> Passive, Exercise –> Obliques (Internal and External), Abdominis (Rectus and Transversus) Internal Intercostals |
Inspiratory Reserve Vol | Air that can be breathed in after normal inspiration |
Tidal Vol | 500mL. Air that moves into the lung on quiet inspiration |
Expiratory Reserve Vol | Air that can still be breathed out after a normal expiration |
Reserve Volume | Air left in lung after maximal expiration |
Inspiratory capacity | TV + IRV |
Function Residual Capacity | RV + ERV |
Vital Capacity | TV + IRV + ERV |
Total Lung Capacity | IRV + TV + ERV + RV |
Physiological Dead Space Definition Calculation | Vol of inspired air that does not participate in gas exchange VD = Anatomical Dead Space of conducting airways + functional dead space in alveoli VD = TV [(PaCO2 -PECO2)/PaCO2] Taco Paco Peco Paco |
Largest contributor to functional dead space? | Apex of Lung |
The tendency is for the lung to … and for the chest wall to … | Lung wants to collapse, Chest wall wants to spring outward |
@ FRC: What is happening with the lung - chest wall system? What is the P in the alveoli and airway? What is the P in the Intrapleural space? | @ FRC: Inward pull of lung = outward pull of chest wall and system pressure is atmospheric. P in the alveoli and airway = 0. P in the Intrapleural space is negative to prevent pneumothorax |
Alveolar transmural pressure is … | Always positive. Meaning always tending to collapse |
What determines the elastic properties of both the chest wall and lungs? | Their combined volume |
What is compliance? What increases compliance? What decreases compliance? | Change in lung vol for a given change in pressure Increases in emphysema and normal aging Decreases in fibrosis, pneumonia and edema |
Hemoglobin Composed of Exists in 2 forms Exhibits | Composed of 2 alpha and 2 beta subunits Exists in Taut form in tissues (low affinity) and Relaxed form in lungs (high affinity) Exhibits positive cooperativeity and negative allostery |
What shifts Hemoglobin dissociation curve to the R (towards T form) | CADET! Turn R! | CO2 and Cl, Acidosis and Altitude, BPG, Exercise, Increased Temp |
Fetal Hemoglobin Consists of Different affinities? | Consists of 2 alpha and 2 gamma subunits | Lower affinity for BPG = higher affinity for O2 --> curve shifted to the L |
Methemoglobin What is it ? Change in affinity? Shift in curve? Treat with | Oxidized Iron 3+ (ferric) instead of Iron 2+ (ferrous) Lower affinity for O2, Higher affinity for cyanide Shifts curve to R Treat with Methylene Blue |
Nitrite poisoning causes | Oxidization of Fe2+ to Fe3+ |
How to treat cyanide poisoning? | Use nitrites to oxidize Hemoglobin to methemoglobin. MetHem with bind cyanide and allow cytochrome oxidase to function. Then use Thiosulfate to bind cyanide --> forms thiocynate which is renally excreted |
Carboxyhemoglobin What is it Affect on O2 binding curve | Hemoglobin bound to CO | Shifts curve to L --> decreased O2 unloading in tissues |
Appearance of Hemoglobin O2 binding curve? | Sigmoidal because of cooperativity |
Pulmonary Circulation Re Resistance and Compliance | Low Resistance and High Compliance |
How does a decrease in PA02 (= increase in PACO2) affect pulmonary circulation? | Vasoconstriction to shift blood away from poorly ventilated areas |
Which gases are perfusion limited? What does that mean? | O2 (normally), CO2, N2O. Diffusion Increases if Blood Flow Increases |
Which gasses are diffusion limited? What does that mean? | O2 (in fibrosis or emphysema), CO. Gas does not equilibrate by the time the blood reaches the end of the capillary. |
Gas diffusion equation What happens in Emphysema? What happens in Fibrosis? | Vgas = (A/T) x D(P1-P2) Emphysema --> Area decreases Fibrosis --> Thickness increases |
Pulmonary artery pressure: Normal? PHTN? | Normal: 10-14mmHg, PHTN: >/= 25 (rest) or >/= 35 (exercise) |
PHTN affect on pulmonary artery | Arteriosclerosis, Medial Hypertrophy, Intimal Fibrosis |
Cause of Primary PHTN | Inactivation of BMPR2 gene which normally functions to inhibit vascular smooth muscle proliferation |
What causes secondary PHTN? What is the course of the disease? | COPD (destruction of lung parenchyma), Mitral Stenosis (Increased resistance --> increased P), Recurrent thromboemboli (decreased cross sectional area of pulmonary vascular bed), autoimmune disease, L --> R shunt (increased sheer stress --> endothelial injury), Sleep Apnea, Living at high altitude Respiratory distress --> Cyanosis and RVH --> cor pulmonale --> death |
Pulmonary Vascular Resistance formula | PVR = (P pulmonary artery - P left atrium) / CO |
O2 content of blood formula | What is normal O2 binding capacity? | O2 binding capacity x saturation + dissolved O2 | O2 binding capacity normally 20ml/dL |
1g Hb can bind how much O2? How much Hb is normally in blood? When does cyanosis occur? | 1.34m Cyanosis occurs when deoxygenated Hb > 5g/dL |
What happens to O2 content of blood, O2 sat and PaO2 when Hb decreases? | O2 content decreases but O2 sat and PaO2 remain the same |
Formula for oxygen delivery to tissues | CO x O2 content of blood |
Alveolar gas equation | PAO2 = PIO2 - PaCO2/R PAO2 = 150 - PaCO2/.8 R = CO2 produced/O2 consumed |
A-a gradient Normal value Increased in? Causes? | Normal A-a gradient = 10-15mmHg Increased in hypoxemia due to lesion in Lung Causes: Shunting, V/Q mismatch, Fibrosis |
Causes of hypoxemia with normal A-a gradient? | High altitude, hypoventilation |
What causes hypoxemia with increased A-a gradient? | V/Q mismatch, Diffusion limitation, R-L shunt |
Causes of Hypoxia | Decreased cardiac output, Hypoxemia, Anemia, CO poisoning |
What can cause ischemia? | Arterial flow or venous drainage blocked |
V/Q at apex? base? | apex = 3 (wasted ventilation). base = .6 (wasted perfusion) |
Where in the lung is ventilation greatest? Where is perfusion greatest? | Both at base |
What happens to V/Q during exercise? | Vasodilation of apical capillaries --> V/Q approaches 1 at apex |
What kind of organisms thrive in the apex of the lung? | Those that thrive on high O2 like TB |
V/Q = 0 | Shunt (airway obstruction). 100% O2 wont help |
V/Q = infinity | Blood flow obstruction (physiological dead space) Assuming <100% dead space, O2 will help |
PAO2, PaO2, and PvO2 in apex, middle and base | Apex: PA>Pa>Pv Middle: Pa>PA>Pv Base: Pa>Pv>PA |
In what forms is CO2 transported in the blood? | Bicarb: 90%, CarbaminoHb (binds at N terminus and binding favors T form): 5%, Dissolved CO2: 5% |
How does oxygenation of Hb affect CO2 in blood? | Oxygenation --> dissociation of H from Hb. H + bicarb = CO2 thus more CO2 is released from RBC Haldane Effect |
Bohr Effect | Increased H in periphery --> Hb O2 curve shifted to R and O2 unloading favored |
Response to high altitude? | Increased Mito, Increased renal excretion of bicarb (to combat alkalosis) Increase in ventilation, decreased PO2 + PCO2, Increased EPO --> Increased Hb and Hc, Increased BPG, RVH "Mr. V. Deb" |
Response to exercise CO2 production O2 consumption Ventilation V/Q Pulmonary blood flow pH PaO2, PaCO2, venous CO2, venous O2 | CO2 production increases, O2 consumption increases, Ventilation increases, V/Q becomes more uniform, Pulmonary blood flow increases, pH decreases (lactic acidosis), PaO2 NC, PaCO2 NC, venous CO2 increase, venous O2 decreases |
DVT What predisposes to it? What can it lead to? Physical Exam sign? Treatment and prevention? | Virchow's triad of Vascular damage (exposed collagen), Increased coagulability (defect in coagulation cascade, most commonly factor V Leiden), Reduced flow [VIR] Leads to Pul embolus Homan's Sign --> Dorsiflexion of foot --> calf pain Heparin for prevention and acute management. Warfarin for long-term prevention of recurrence |
Sudden onset of dyspnea, chest pain, and tachypnea | Pulmonary embolism |
Types of PE? | FAT BAT | Fat, Air, Thrombus, Bacteria, Amnionic fluid, Tumor |
Fat embolus associated with… | Presents as… | Long bone fracture and liposuction | Presents as hypoxemia, neurological abnormalities, petechial rash |
Major risk with Amnionic fluid embolus? | Can lead to DIC especially post partum |
Imaging test of choice for PE? | CT pulmonary angiography |
Where do most PEs arise from? | 95% from deep leg veins |
Most dangerous location for PE? | Saddle Embolus of Pulmonary Artery |
Histology of thromboembolus formed premortem? | Lines of Zahn: interdigitating areas of pink (platelets, fibirn) and red (RBCs) |
Obstructive Lung Disease: Names, RV, FVC, PFTs, V/Q, PO2, PCO2 | Chronic Bronchitis, Emphysema, Asthma, Bronchiectasis RV: Increases, FVC: Decreases FEV1 decrease, FVC decreases, FEV1/FVC decreases V/Q decreases, PO2 decreases, PCO2 increases |
Chronic Bronchitis: Clinical definition | Productive Cough for >3 months (not necessarily consecutive) for >2 years |
Chronic Bronchitis: Pathology and Physical Findings | Harry Reid Won 50% Securing Complete Democratic Control Hypertrophy of Mucus secreting glands in bronchi, Reid Index > 50%, Wheezing, Small airway disease, Crackles (early) Dyspnea (late), Cyanosis (early onset hypoxemia due to shunting) |
Emphysema: pathology and findings | PERCE Pursed lip breathing (increased airway pressure prevents collapse), Enlarged airspace, Recoil decreased, Compliance increased, Elastase activity increased |
Two types of emphysema | Centriacinar = smoking Panacinar = alpha-1-antitrypsin deficiency |
Alpha Agonists Names Uses Tox | Pseudoephedrine, Phenylephrine Reduce hyperemia, edema, nasal congestion. Open up Eustachian tube. Pseudoephedrine is a stimulant. Can cause HTN. Pseudoephedrine can cause CNS stimulation/anxiety |
Dextromethorphan Class MoA Uses Risk Antidote | Opioid (synthetic codeine analog) Antagonizes NMDAR Antitussive Mild abuse potential Naloxone treats OD |
Bosentan MoA Uses | Competative antagonist of endothelin 1 receptor Decreases Pulmonary Vascular Resistance Used to treat Pulmonary Arterial HTN |
N Acetylcysteine Type of drug Action Uses | Mucolytic expectorant Loosens mucus plugs in CF Antidote for acetaminophen OD |
Guaifenesin Type of drug Action | Expectorant that thins the respiratory secretions but does not suppress the cough reflex |
Molecules that cause bronchoconstriction? | Adenosine, ACh |
Molecules that cause Bronchodilation | cAMP |
Ab Asthma therapy Name MoA Uses | Omalizumab Monoclonal IgE Ab that binds up serum IgE Used in allergic asthma resistant to steroids and long acting beta2 agonists |