The Black Lung Flashcards

Question

Answer 1

Bacterial Pneumonia: Classify based off organism: Staph or Strep Classify based by distribution: Bronchopneumonia, Lobar pneumonia Alveolar spaces are filled by neutrophils, fibrin, RBCs, and macrophages. Alveolar septa are typically hyperemic and congested but not inflamed.

Answer 2

*Streptococcus pneumoniae*

Answer 3

gram-negative bacilli (*Pseudomonas, Klebsiella, Proteus, E. Coli*) reach patients lungs via upper airways or through the blood

Answer 4

*Staphylococcal* and *Haemophilus*

Answer 5

*Legionella pneumophilia* Multiple small abscesses are frequent. Organism is NOT seen on a Gram stain, grows only on special culture media --\> Diagnosis is easily missed!

Answer 6

**Lung Abscess** (associated w/ bronchial obstruction, Anaerobes) **Emphysema** (infection in the pleural space) **Organization** ("Organizing Pneumonia") - formation of granulation tissue in the alveoli (*Masson bodies*) **Dissemination of infection** (bacteremia w/ sepsis)

Answer 7

usually **viral**, following URI (Influenza, Adenovirus, Measles, Varicella) \*most common cause of pneumonia in children Clinical: Dry, hacking cough, fever, headache, muscle ache

Answer 8

Viral: inflammation in the alveolar septa. Mononuclear infiltrate, the septa is widened and edematous, w/ hyperplasia of the Type II pneumocytes, alveolar walls may be lined by hyaline membranes. Viral inclusions may be visible, depending on the virus. Bacterial: alveolar spaces filled w/ neutrophils, macrophages, fibrin, RBCs. Septa hyperemic, but not inflammed.

Answer 9

spreads from spores in the dust (southwest) causes Granulomatous inflammation w/ giant cells and macrophages

Answer 10

Fungal infection caused by *Histoplasma*, usually innocuous unless in immunocompromised Mississippi and Ohio River valleys; spreads from spores in the dust causes granulomatous inflammation w/ necrosis at center --\> nodules

Answer 11

Fungal infection caused by *Blastomyces* inhalation thru dust in eastern U.S. mixed acute and granulomatous inflammation; large years w/ broad-based budding

Answer 12

Coccidioides Histoplasma Blastomycosis Mycobacterium tuberculosis

Answer 13

spread person-to-person; prison/immigrants Causes Primary complex: granulomas in lung AND hilar lymph nodes ("Ghon complex"), frequently calcify Secondary (reactivation): granulomas in other organs

Answer 14

Immunocompromised: AIDS, Leukemia/Lymphoma, Heriditary immunologic disorders, Chemotherapy, Organ/Bone Marrow transplant, Steroid therapy (long-term, high dose) Fungi: *Pneumocystis, Aspergillus, Zygomycetes, Cryptococcus, Candida* Viruses: *Cyteomegalovirus, Herpes Simplex* Bacteria: *Actinomyces, Nocardia*

Answer 15

Conducting portion Respiratory portion

Answer 16

nasal cavity, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles F(x): delivers air to the respiratory portion, filters the air to remove dust, debris, warms to room temp/humidifies. Nose participates in olfaction, helps resonate the voice

Answer 17

respiratory bronchioles, alveolar ducts, alveolar sacs, alveoli F(x): enable gas exchange b/w air and blood

Answer 18

pseudostratified columnar ciliated epithelium (supported by hyaline cartilage) superior (false) vocal cords: pseudostratified Inferior (true) vocal cords: stratified (core *vocalis* muscle - phonation)

Answer 19

Pseudostratified columnar ciliated epithelium w/ goblet cells Seromucous glands C-shaped hyaline cartilage ring w/ trachealis (sm. muscle)

Answer 20

fluted epithelium (NOT respiratory epithelium) no cartilage no Seromucous glands ciliated simple columnar epithelium w/ Clara cells Smooth Muscle relatively prominent \*Bronchioles involved in asthma - sm. muscle is hyperactive --\> increased Goblet cells, glands, and sm. muscle

Answer 21

goblet: produce mucus brush: innervated and serve sensory function basal: renew the epithelium

Answer 22

Type II pneumocytes In premature infants --\> their lungs are immature and do not produce enough surfactant. This prevents the babies from breathing normally and causes **respiratory distress syndrome**.

Answer 23

Air blood barrier: Gas must cross the endothelial membrane --\> basal lamina --\> pnuemocyte type I cell membrane

Answer 24

**lecithin- sphingomyelin (L/S) ratio** in amniotic fluid (≥ 2 is healthy; \< 1.5 predictive of NRDS), \*Persistently low O2 tension risk of PDA. Neonatal Respiratory Distress Syndrome --\> supp. O₂--\> Bronchopulmonary dysplasia

Answer 25

Esophagotracheal fistula Typically this is a failure of the splanchnic mesoderm to push apart the endodermal tubes and is thus associated with other mesodermal malformations Unable to take milk into the stomach, respiratory issues

Answer 26

inferior of rib (costal groove) chest tube above rib, if below then likely nerve damage

Answer 27

**Lungs**: lymph upward --\>right lymph duct--\> thoracic duct --\> R/L subclavian vein Cancer metastasize --\> supraclavicular lymph nodes **Chest wall:** lymph lateral --\> axilla breast metastasis --\> axilla lymph nodes

Answer 28

room for lung expansion during inspiration

Answer 29

inferior lobe of the right lung Right is wider and more vertical than Left side

Answer 30

bronchioles

Answer 31

Pulmonary arteries branch with the airway and supply the alveoli with vessels for gas exchange. Larger airways have a separate blood supply arising from the aorta, i.e. the ***bronchial arteries***. Pulmonary veins do not follow the airways but do exit the lungs at the hilus.

Answer 32

SNS: bronchodilation, vasoconstriction, decreased mucus secretion. The postganglionic fibers originate in sympathetic chain ganglia in the superior cervical ganglion to the T5 sympathetic ganglion.

Answer 33

PNS: bronchoconstriction, vasodilation, increased mucus secretion. vagus nerve

Answer 34

= RR x VT Respiratory Rate x Tidal Volume

Answer 35

CO₂ output/ O₂ uptake R(exchange ratio) is measured; RQ is inferred determined by the tissues metabolic rate

Answer 36

= Elastic Recoil Pressure / Upstream Airway Resistance

Answer 37

1. abrupt decline in respiratory function 2. bilateral infiltrates 3. reduced lung compliance 4. hypoxemia 5. absence of heart failure

Answer 38

any agent that diffusely injures the lung parenchyma (sepsis, aspiration, infections, trauma, radiation, inhalation of toxic agents, drug reactions)

Answer 39

When the cause of **ALI** is idiopathic

Answer 40

a _clinical syndrome_ characterized by severe acute respiratory failure, and is a manifestation of severe ALI. \*Not all ALI is severe enough to become ARDS

Answer 41

_pathologic term_ and is the histologic manifestation of severe ACI, and generally occurs in association with clinical ARDS. Gross: Lungs heavy, firm, red-tan appearance endothelium injury w/ endothelial activation --\> recruit neutro --\> accumulate fluid in alveolar spaces --\> form hyaline membranes --\> release cytokines that perpetuate inflammatory response. Microscopic: Diffuse damage to all parts of Alveoli (epi/endothelium), formation of "hyaline membranes" on alveoli surface, Hyperplasia of Type II pneumocytes, Granulation tissue formation w/ influx of lymphocytes, macrophages, fibroblasts.

Answer 42

The result of epithelial or endothelial injury (or both) Causes: sepsis; diffuse pulmonary infections; aspiration; trauma Endotoxin release in sepsis, release of TNF-alpha, and injury from microthrombi High protein pulmonary edema, leaking across major gaps into the alveoli

Answer 43

ARDS: syndrome of decreased *arterial oxygen*; decreased *lung compliance*; diffuse pulmonary infiltrates on radiographs; without primary left-sided heart failure. History of catastrophic event with acute respiratory failure DAD: **pathologic** name for ARDS based off the following microscopic features: alveolar endothelial and epithelial injury; hyaline membranes; pneumocyte type II cell hyperplasia; and the host response of lymphocytes, macrophages, and sometimes fibrosis

Answer 44

Gross: lung is heavy, firm, red-tan appearance Micro: Hyaline membranes, type II pneumocyte hyperplasia, inflammation microscopically

Answer 45

idiopathic Fibrosis only involves the lungs M \> W; older adults smoking, fumes, dust, occupational irritants Familial forms Path: unregulated fibrosis rather than inflammation --\> more collagen --\> death Gross: small lungs, bumpy pleura, "honeycombing" Micro: dense fibrosis, "spatial heterogeneity", areas of dense mature fibrosis next to losse immature fibrosis

Answer 46

_pathological pattern_ of fibrosis, characterized by heterogenous and peripherally accentuated fibrosis. This pattern may be seen in IPF if its cause is idiopathic, but the UIP pattern may also be seen in other non-idiopathic conditions. IPF = idiopathic IF _UIP_ is observed, then must exclude other known causes before clinical diagnosis of _IPF_

Answer 47

*Prognosis is worse than for all other types of chronic interstitial lung disease* most die within 3-4 years after initial diagnosis

Answer 48

- diffuse interstitial infiltrates - relatively mild upper respiratory symptoms (minimum sputum and low fever); 'atypical' presentation - caused by bacteria or virus

Answer 49

old term for “bronchiolitis obliterans organizing pneumonia” good prognosis steroids used for treatment

Answer 50

* **Systemic disease** characterized by ***noncaseating granulomas*** in multiple organs; classically seen in ***African American females*** * Etiology is unknown; likely due to **CD4+helper T-cell** response to an unknown antigen * Granulomas most commonly involve the **hilar lymph nodes** and lung, leading to restrictive lung disease. Characteristic stellate inclusions ('asteroid bodies') are often seen within giant cells of the granulomas Other commonly involved tissues include the _uvea_ (uveitis), _skin_ (cutaneous nodules or erythema nodosum), and salivary and lacrimal _glands_ (*mimics Sjogren syndrome*); almost any tissue can be involved. Clinical features: Dyspnea or cough (most common presenting symptom); Elevated serum ACE; *Hypercalcemia (1-alpha hydroxylase activity of epithelioid histiocytes converts vitamin D to its active form)* Treatment is steroids; often resolves spontaneously without treatment.

Answer 51

* Granulomatous reaction to inhaled organic antigens (e.g., pigeon breeder's lung) * Presents with fever, cough, and dyspnea hours after exposure; resolves with removal of the exposure * Chronic exposure leads to interstitial fibrosis.

Answer 52

smoking-related interstitial lung disease High [macrophages] within alveolar spaces --\> interstitial fibrosis

Answer 53

another smoking-related interstitial lung disease, closely related to DIP but generally milder, characterized by accumulation of lesser numbers of macrophages within alveolar spaces (compared to DIP), with mild peribronchiolar fibrosis

Answer 54

\*rare accumulation of surfactant within alveolar spaces and bronchioles, from defects in macrophage f(x) or granulocyte macrophage -CSF \*Autoimmune is most common (90%); all 3 involve GM-CSF signaling issues

Answer 55

**CONNECTIVE TISSUE DISEASE-ASSOCIATED INTERSTITIAL LUNG DISEASE** **DRUG-INDUCED LUNG DISEASE** **HYPERSENSITIVITY PNEUMONITIS**

Answer 56

Interstitial fibrosis due to occupational exposure; requires chronic exposure to small particles that are fibrogenic Alveolar macrophages engulfforeign particles and induce fibrosis **ABC's**: asbestos, berylium, coal, silica

Answer 57

small aggregates of coal dust-laden macrophages in terminal bronchioles and respiratory ducts --\> may progress to fibrosis w/ more dust "Anthracosis" - black dust accumulation in lungs (urban metro areas, miners, can progress w/ other enviro factors to "Progressive Massive Fibrosis"

Answer 58

siOH interacts w/ cell membranes --\> Free Radicals generated --\> inflammatory cells accmulate chronically silicotic nodules --\> lymph nodes complicated silicosis --\> silica nodules aggregate into large fibrous masses in lungs

Answer 59

Type IV sensitivity response causes granulomatous disease in the lungs that appears virtually identical to sarcoidosis; granulomas in lymph nodes and systemic organs

Answer 60

Asbestos fibers; seen in construction workers, plumbers and shipyard workers Asbestos + iron + protein = "Asbestos bodies" --\> fibrosis of lung and pleura plaques w/ increases risk for lung carcinoma, mesothelioma; lung carcinoma is more common than mesothelioma in exposed individuals peritoneal mesotheliomas

Answer 61

1 / compliance = ΔP/ΔV = recoil compliance = ΔV/ΔP

Answer 62

Respiratory Resistance = chest wall resistance + lung resistance Lung Resistance = tissue and airway components (90% respiratory resistance) Airway is 80% of lung resistance (upper/central airways) / lung tissue is 20 % of the lung resistance Chest wall only has tissue resistance (10% of TRS resistance)

Answer 63

PE is stored in the lung --\> recoil Expiration: PE stored in lung is transfered to raise alveolar pressure causing gas to flow out of the lung. The recoil Pressure decreases as the volume is exhaled. Low compliance = High inflation pressure with little change in volume compare to normal, healthy lung.

Answer 64

evident only when air is flowing (not static) energy lost due to friction and turbulent gas flow \*no flow --\> no resistance

Answer 65

increase velocity increase radius Pressure = K2(Flow)^2 (K2 is the turbulent flow constant) If flow is doubled, the pressure needed to move the gas increases four times. \*Harder to move turbulent gas

Answer 66

upper airway (mouth, pharynx, larynx) = 30% lower airway = 70%

Answer 67

**peripheral airways** (d \< 2mm) have a **large total cross section** w/ many small airways in parallel --\> low resistance (20%)

Answer 68

Growth: Larger lungs have larger airways (large lungs more compliant) Inspiration: deep breath --\> increase airway diameter --\> higher lung volume --\> lower resistance specific resistance = resistance x lung volume

Answer 69

low lung recoil --\> high resistance emphysema destroys alveolar walls leads to greater RV, lower VC --\> 'barrel chests'

Answer 70

cholinergic acetylcholine histamine/leukotrienes smoke, cold air, SO₂

Answer 71

Adrenergic (Beta₂) Norepinephrine Prostaglandin E

Answer 72

allergic rxn --\> mast cells release histamines, bradykinins, leukotrienes --\> cause airway mucosal edema and mucus production symptoms = albuterol (selective Beta₂ agonist) inflammation = inhaled corticosteroids, leukotriene receptor antagonists

Answer 73

Foreign body (peanuts, sunflower seeds, toys, pen tops etc) Mucus or mucopurulent material  Blood clots in pulmonary hemorrhage  Tumor

Answer 74

* Inflammation (asthma, bronchiolitis, chronic bronchitis, cystic fibrosis, acute bronchitis, aspiration of stomach content/acid, inhalation of chemicals/gases, crouplaryngotracheobronchitis) * Bronchospasm (asthma, aspiration of stomach content/acid, inhalation of chemicals/gases) * Vascular congestion (cardiac asthma) * Tracheobronchomalacia (floppy airways w/ loss or failure to develop cartilaginous  structures) * Tumor * Cysts (particularly in upper airway) * Vocal cord paralysis * Fibrosis/scarring (post lung transplant/airway surgery, sub-glottic stenosis after airway trauma from intubation)

Answer 75

* Lymph nodes at hilum (tumor such as lymphoma, infection such as coccidiodomycosis or TB) * Mediastinal mass (reduplication of esophagus, tumors, bronchogenic cysts) * Vascular sling or ring (aberrant subclavian, pulmonary sling, double aortic arch, right-sided aortic arch) * Cardiac enlargement (esp. left lower lobe) * Neck mass (infection, cystic hygroma, tumor) * Failure of elastic recoil to maintain patency of the small airways (emphysema)

Answer 76

elastance = change P/ change V If lungs are stiffer, then likely higher RV leading to increased elastance

Answer 77

Slow, deep tidal volume will result in higher elastic work during breathing (optimal for increased resistance in obstructive disease)

Answer 78

Fast, shallow tidal volume --\> higher resistive work during breathing (elastance is increased in restrictive disease)

Answer 79

Maximal expiratory flow is independent of effort

Answer 80

FEV1: amount of air exhaled in 1 sec Forced vital capacity: how much air you can breath in fully and breath out fully. FVC + RV = TLC

Answer 81

decreased pulmonary artery pressure from drop in volume --\> vessels collapse --\> decreased cross-sectional area --\> increased resistance --\> Open vessels will close (de-recruitment), and create physiologic dead space that increases as shock worsens

Answer 82

creates hydrostatic pressure gradient --\> higher pressure at base of lung --\> distends vessels --\> decreases resistance to blood flow thus, base of lung naturally recieves more blood than apex

Answer 83

intraalveolar vessels (high alveolar pressures compress the vessels) resistance is low extraalveolar vessels, which are distended with blood.

Answer 84

high in the extraalveolar vessels (the vessels collapse) resistance is low in the intraalveolar vessels (they remain open because alveolar pressure is lower).

Answer 85

FRC, because this is right in the middle (the sum of the resistances is the lowest). This is the range in which we normally maintain lung volume.

Answer 86

vasoconstricts This shunts blood flow away from this region to an area with normal ventilation, and helps to maintain normal oxygen saturation Acidosis, hypercapnia, and smooth muscle hypertrophy accentuate the response to hypoxia

Answer 87

thromboxane A2 histamine angiotensin

Answer 88

prostacyclin acetylcholine bradykinin

Answer 89

increased P_H (cardiogenic pulmonary edema) inside the pulmonary capillaries that leads to a greater volume of fluid leaving the blood stream. (mitral valve stenosis, left atrial tumor, left ventricular failure, fluid overload due to renal failure) non-hydrostatic (non-cardiogenic) pulmonary edema --\> increased capillary permeability --\> increased fluid/protein leaving the vasculature (chemical inhalation, drowning, smoke inhalation, endotoxin, shock, head injury)

Answer 90

Measured when the patient inspires to total lung capacity, then exhales as rapidly and forcefully as possible until residual volume is reached. If enough force is used, dynamic airway compression is caused and flow limitation is reached.

Answer 91

the forced expiratory volume in one second. It is a measure of how rapidly the subject can exhale (the flow obtained). FEV1/FVC is the percent after correcting for lung volume and is normally \>72% in adults

Answer 92

the forced expiratory flow from 25 to 75% of vital capacity. This averages flow over the middle of the FVC, and assesses lung function determined by the peripheral airways more than FEV1. It can detect the early onset of diseases like emphysema and cystic fibrosis, which damage the peripheral airways.

Answer 93

Proportional to pulmonary elastic recoil at that volume inversely proportional to the resistance of the airways at that lung volume. \*It is independent of the chest wall effort once adequate effort has been achieved

Answer 94

-an abnormal collection of fluid in the pleural space * High fluid production (by systemic vessels in visceral and parietal pleura) * Low elimination of fluid (mostly via absorption by lymphatics in parietal pleura)

Answer 95

* High capillary hydrostatic pressure in systemic and/or pulmonary circulation (e.g., **CHF**) * Low intravascular oncotic pressure (e.g., **hypoalbuminemia, cirrhosis**) * High capillary permeability or vascular disruption (e.g., **malignancy, inflammation, infection, pancreatitis**) * Low lymphatic drainage/blockage, including thoracic duct obstruction or rupture (e.g., **malignancy, trauma**) * High peritoneal fluid --\> migration across diaphragm via lymphatics or structural defect (e.g., **cirrhosis w/ ascites**)

Answer 96

Symptoms: Dyspnea - most likely from altered mechanics, Chest pain - if inflammation, Cough, PE findings (significant effusion \>250ml): Decreased expansion, Dullness to purcussion, Decreased breath sounds and decreased tactile fremitus, tracheal deviation, plueral friction rub

Answer 97

* Imaging * **CXR** or chest CT – dense meniscus around lung (esp. obscuring corners at diaphragm) * US – confirm effusion is not atelectasis and direct thoracocentesis * **Thoracentesis** (pleural effusion analysis) – distinguish transudate vs. exudate * transudate (CHF, hypoalbuminemia, nephrotic syndrome, cirrhosis) * Exudate (infection, malignancy, inflammation)

Answer 98

autosomal recessive most common genetic disease amongs whites (european descent) **CFTR gene** - F505 deletion = most common

Answer 99

Epithelial Chloride channel - inhibit ENaC regulates outwardly rectifying chloride channel regulates ATP channels \*the mutation leads to poor solubility and aggregation of mucus in the lumen.

Answer 100

upper pons ends inspiration --\> control **tidal volume and RR** not necessary for normal breathing \*Damage --\> apneustic breathing

Answer 101

lower pons signals DRG --\> High duration of excitatory ramping of diaphragmatic activity **apneustic breathing** - damage above APC --\> prolonged inspiratory gasps terminated by a brief, rapid expiratory effort

Answer 102

inspiration controls basic rhythm of breathing - cycles of quiescence and crescendo input: CN X and IX thru NTS pneumotaxic center --\> ends inspiration --\> shorter, shallow breaths apneuistic center --\> High duration of excitatory ramping of diaphragmatic activity

Answer 103

expiration not active during quiet (normal) breathing (passive inspiration) exercise --\> rhythm by pre-Botzinger complex

Answer 104

respond to CO2, O2, pH (H⁺) High PaCO2 --\> CO2 uncharged into CSF --\> H2O+CO2 --\> HCO3^-+ H⁺ **= Low pH --\>** stimulates HIGH ventilation linear response (2X CO2 --\> 2X ventilation) responsible for 80% of response to PaCO2 _suppressed by hypoxemia_ (High CO2 affinity)

Answer 105

carotid bodies and aortic arch respond to **hypoxia** (PaO2 \< 50mmHg), hypercarbia or **acidemia** responsible for 20% of response to PaCO2

Answer 106

1. Deep breath to load the lung. 2. The glottis is closed and the abdominal muscles are contracted to pressurize the air. 3. The glottis opens rapidly and the air is expelled at a high velocity. 4. The high velocity moves phlegm up through propulsion, aerosolization, and wave movement.

Answer 107

Reynold's #: Increased gas density = Increased _turbulence_ ==\> **High Resistance** Adding a _low density_ gas will *decrease turbelence and work of breathing* Turbulent: **Pressure = flow²** Laminar: **Pressure = flow**

Answer 108

Pressure outside _extrathoracic_ airway greater than in airway lumen Collapse on inspiration = **inspiratory stridor**

Answer 109

Pressure outside _intrathoracic_ airway greater than in airway lumen Collapse on expiration = **expiratory wheeze**

Answer 110

pO2 \< 60 mmHg w/ a normal or low pCO2 Where the oxyhemoglobin dissociation begins to fall rapidly

Answer 111

pCO2 \> 50 mmHg secondary to a decrease in the alveolar ventilation that results from either a decrease in the minute ventilation (TV x RR) or an increase in the dead space (doesn't eliminate CO2) or both. \*lower pH in acute hypercapnia prior to renal compensation

Answer 112

**_V/Q mismatch_**: Low V/Q units cause hypoxemia and hypercapnia. Supplemental oxygen eliminates the low V/Q units and corrects the hypoxemia **_Shunt_**: persistence of hypoxemia despite 100% oxygen. Occurs in pneumonia, atelectasis, and severe pulmonary edema, VSD/ASD, patent ductus arteriosus, *bronchial & thebesian circulations* **_Hypoventilation_**: due to obstructive lung disease, upper airway obstruction, chest wall abnormalities, CNS depression, neuromuscular disease. Hypercapnia and hypoxemia. Alveolar-arterial pO2 gradient is normal **_Diffusion Limitation_**: thickening of the alveolar septa will create a greater difference between alveolar and arterial oxygen levels (pO2). This can cause hypoxemia

Answer 113

Inability to speak in phrases or full sentences Use of accessory muscles to breathe Pulsus paradoxus \>25 mmHg Eucapnia or hypercapnia “Quiet” chest Altered mental status

Answer 114

No tracheal deviation Increased fremitus Dull or flat to percussion Bronchial breath sounds (consolidation conducts more sound) Audible crackles Egophony

Answer 115

Left sided HF --\> Increased pulmonary P_H --\> drive fluid out of capillaries into the interstitial space

Answer 116

Diffuse damage to the alveolar-capillary interface Leakage of protein-rich fluid leads to edema that combines w/ necrotic epithelial cells to form **hyaline** membranes in alveoli ==\> activation of neutrophils induces protease- and free radical-mediated damage of type I and II pneumocytes Causes: sepsis, shock, infection treat: address underlying cause; Ventilation w/ PEEP \*increases diffusion barrier; eventually R --\> L shunt

Answer 117

Emphysema/Primary Pulmonary HTN --\> RV hypertrophy (chronic) or dilated (acute) Causes: COPD, pulmonary interstitial fibrosis, pneumoconioses, CF, bronchiectases, PE, pulmonary vascular constriction (metabolic acidosis, hypoxemia) Symptoms: dyspnea on exertion, fatigue, ankle swelling. Possible holosystolic murmur (tricuspid). Elevated JVP. Splitting of S2. Heptomegaly

Answer 118

COPD patients are hypercapnic and hypoxemic. Supp. O2 can help hypoxemia, eliminating low V/Q units

Answer 119

The alveolar air equation can help determine the cause of hypoxemia. It can also help to determine if supplemental oxygen is needed. If the alveolar-arterial pO2 gradient is normal, then the cause is due to hypoventilation. If the gradient is not normal, then the hypoxemia is related to another cause, such as V/Q mismatch or shunt.

Answer 120

Chronic hypercapnia leads to CO2 diffusing into the brain and producing carbonic acid, which dissociates into bicarbonate and H+. If enough bicarbonate forms, then a buffer forms in the CSF. This buffer causes the chemoreceptors to reset their set point; they become less sensitive to changes in pH and are unable to effectively modify ventilation in response to increases in pCO2. Due to the respiratory acidosis, the kidneys will compensate by reabsorbing more bicarbonate, thus increasing the pH (metabolic alkalosis). This inhibits the peripheral response to acidemia and carbon dioxide levels. The only driving force now for ventilation is the hypoxemia. If supplemental oxygen is given at too high of levels, then the patient will stop breathing. *Haldane effect*: hypoxemic vasoconstriction also play a role in this effect.

Answer 121

In patients with respiratory failure, the positive pressure ventilation can help to keep their lungs open and may allow them their hypoxemia to be corrected, especially since the patient cannot adequately ventilate themselves. The positive pressure keeps the lung open and prevents shunt (which is very hard to improve on supplemental oxygen alone). BPAP indicated to allow for CO2 blow off (ventilation) (Hypercapnic) CPAP can be used in patients who are just hypoxemic