The Black Lung Flashcards
Tidal Volume (TV)
amount of air exchanged w/ each breath = 7 ml/kg normally
Residual Volume (RV)
volume of gas left in lung after a complete expiration = 25% of total lung capacity (TLC)
Inspiratory Reserve Volume (IRV)
How do you calculate?
volume of air that can be inspired from end of tidal inspiration to total lung capacity = IC – TV
Expiratory Reserve Volume (ERV)
volume of air that we can exhale from end of a tidal expiration to residual volume –> forcibly exhale
Total Lung Capacity (TLC)
= total volume of gas in lung at end of maximal inspiration = sum of all above volumes (RV + ERV + TV + IRV)
volume at which inward (expiratory) recoil of the lung and chest wall > strength of inspiratory muscles
Vital Capacity
= TLC – RV = volume of air that can be exhaled from total lung capacity to residual volume = 75% of total lung capacity measurement – inspire completely and then expire VC into spirometer
Functional Residual Capacity (FRC)
RV + ERV
volume of gas in the lungs after normal expiration
Inspiratory Capacity (IC)
= TLC – FRC = TV + IRV = amount of gas we can inspire from functional residual capacity to total lung capacity.
Elastic Properties of the Lung (3)
transpulmonary pressure = alveolar pressure – pleural pressure
compliance
recoil forces: tissue (elastin/collagen) and surface tension
How does lung compliance change with Greater lung volume and growth
HIGH volume in lung (inspiration) –> LOW compliance
HIGH lung volume (size of lung) –> HIGH absolute compliance
*an adult is more compliant than a child
Function of surfactant
What happens when there is none?
Surfactant: prevents collapse of alveoli and allows them to stretch open more easily, thus stabilizing the lung
Small alveolus (small radius), surfactant breaks up (reduces) the surface tension
Large alveolus (large radius), surface tension is greater because the surfactant is diluted by the larger surface area
Premature infants have no surfactant –> alveoli collapse. Cannot generate enough inspiratory pressure to overcome surface tension –> respiratory distress syndrome
Elastic properties of the chest wall
- resting volume of chest wall = 70% of TLC
- outward recoil force on lung at FRC (40% TLC) aids inspiration
- inward recoil of force at >70% TLC aids expiration
Elastic properties of the total respiratory system (chest wall + lungs)
- lung always wants to deflate
- chest wall wants to expand (except at highest volumes)
- total lung capacity (TLC) = point at which muscles can no longer overcome expiratory recoil of lung + expiratory recoil of chest wall
- functional residual capacity (FRC) = balance of outward recoil of chest against inward recoil of lung
How does gravity work in causing regional ventilation differences b/w apex and base of lung?
-
pleural pressure gradient (more P at base) – weight of lung increases pressure on plural space as you go down
- more negative pressure (less pressure) at apex –> High transpulmonary pressure (PL) –> alveoli are bigger (higher percent of max size) and stiffer
-
regional ventilation
- High size of base alveoli –> High compliance –> High ΔP during inhalation –> High ventilation
- matches High perfusion at base of lung
What is pulmonary hypertension
pulmonary arteriole HTN?
Resting MAP of >25 mmHg (right heart catheterization)
PAH adds to the criteria that pulmonary venous pressure (or capillary wedge) must be <15 mmHg
Equation for pulmonary arteriole pressure
PA mean = (CO x PVR) + PCWP
Determined by:
Right-sided CO
Pulmonary vascular resistance
Mean pulmonary venous pressure/left atrial pressure (PCWP)
What medical conditions lead to increases in Pulmonary venous pressure? (pulmonary HTN)
LV dystolic/systolic dysfunction
mitral valve disease –> increase pulmonary venous pressure
What medical conditions lead to increases in Pulmonary vascular resistance? (pulmonary HTN)
any condition that decreases the area of the pulmonary vascular bed (pulmonary emboli, C.T. diseases, interstitial lung disease, COPD)
or induce hypoxic vasoconstriction (any lung disease producing hypoxia) increases pulmonary vascular resistance
What medical conditions lead to increases in Right-sided cardiac output? (pulmonary HTN)
Left-to-right atrial septal defects (ASD)
Left-to-right ventricle septal defects (VSD)
other systemic-to-pulmonary shunts
overall, increase right-sided CO by increasing RV volume
What are the 3 abnormal signaling pathways in pulmonary HTN?
Prostacyclin: Arachidonic acid –> cAMP –I Ca2+ entry into sm. muscle cell –> vasodilation, antiproliferation.
NO: forms NO from arginine –> guanylate cyclase(GTP–>cGMP) –I Ca2+ entry into sm. muscle cell –> vasodilation, antiproliferation
Endothelin: forms ETA and ETB –> vasoconstriction, proliferation
Pulmonary HTN: decreased Prostacyclin, NO and Increased Enothelin
Ways to treat pulmonary HTN based off of the 3 altered pathways
Calcium channel blockers
Prostacyclin analogs (Low prostacyclin synthase)
Sildenifil (PDE5 inhibitors): promote activity of NO pathway
Endothelin receptor antagonists block the effect of endothelin at sm. muscle cell receptors
What are the general types of pneumonia
Community-acquired pneumonia: 95% viral
Nosocomial pneumonia: hospital-acquired (gram negative)
Aspiration pneumonia: mix of anaerobic/aerobic bacteria
Pnemonia in immunosuppressed patient: HIV, leukemia, lymphoma, chemotherapy, iatrogenic immunosuppresion
May be categorized based off of organism
Pathogenesis of Pneumonia (5)
Loss of defense:
- inhibition of the normal cough reflex (neuromuscular disease, drug overdose, intubation, coma)
- injury of mucociliary apparatus (viral destruction, smoking, genetic disease - immotile cilia syndrome)
- interference of phagocytic or bactericidal action of alveolar macrophages (alcohol, tobacco smoke, anoxia)
- bronchial obstruction (neoplasm, mucus plugging)
- decreased immunity (immunodeficiency, viral infections, leukemia, lymphoma, immunosuppressive therapy, chemotherapy)
Bacterial pneumonia: Gram-positive cocci
Alveolar spaces are filled by neutrophils, fibrin, RBCs, and macrophages. Alveolar septa are typically hyperemic and congested but not inflamed.
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.
Most common organism causing pneumonia in ambulatory patients?
Streptococcus pneumoniae
Most common organism causing pneumonia in hospitalized patients?
gram-negative bacilli (Pseudomonas, Klebsiella, Proteus, E. Coli)
reach patients lungs via upper airways or through the blood
What organisms often follow upper respiratory viral infections?
Staphylococcal and Haemophilus
What is associated w/ aerosols from old AC units (resistant to chlorine)
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!
Complications of Bacterial Pneumonia
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)
Atypical Pneumonia
usual pathogens
Presentation
usually viral, following URI (Influenza, Adenovirus, Measles, Varicella)
*most common cause of pneumonia in children
Clinical: Dry, hacking cough, fever, headache, muscle ache
How does viral pneumonia differ from bacterial pneumonia?
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.
Coccidiodomycosis (“Valley Fever”)
spreads from spores in the dust (southwest)
causes Granulomatous inflammation w/ giant cells and macrophages
Histoplasmosis
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
Blastomycosis
Fungal infection caused by Blastomyces
inhalation thru dust in eastern U.S.
mixed acute and granulomatous inflammation; large years w/ broad-based budding
Common Fungi and Mycobacterial infections that cause pneumonia
Coccidioides
Histoplasma
Blastomycosis
Mycobacterium tuberculosis
Tuberculosis
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
People at risk for opportunistic infections:
Common organisms:
Fungi (5)
Viruses (2)
Bacteria (2)
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
2 major divisions of the Respiratory System
Conducting portion
Respiratory portion
Conducting portion of the Respiratory System consists of:
what is its function?
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
Respiratory portion of the Respiratory System consists of:
what is its function?
respiratory bronchioles, alveolar ducts, alveolar sacs, alveoli
F(x): enable gas exchange b/w air and blood
Epithelial lining of the Larynx
pseudostratified columnar ciliated epithelium (supported by hyaline cartilage)
superior (false) vocal cords: pseudostratified
Inferior (true) vocal cords: stratified (core vocalis muscle - phonation)
Epithelial lining of the Trachea
Pseudostratified columnar ciliated epithelium w/ goblet cells
Seromucous glands
C-shaped hyaline cartilage ring w/ trachealis (sm. muscle)
Contents of Bronchioles
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
Function of:
Goblet cells
Brush cells
Basal cells
goblet: produce mucus
brush: innervated and serve sensory function
basal: renew the epithelium
What produced surfactant
Who doesn’t have surfactant?
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.
Air blood barrier: Gas must cross the endothelial membrane –> basal lamina –> pnuemocyte type I cell membrane
How to screen fetal lung maturity
2 complications of premature birth - congenital
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
malformation of the lung buds and foregut can produce an aberrant connection known as ______
What embryonic process occurs to cause this
What will newborn present as?
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
Where is the neurovascular bundle located?
Why is this clinically important
inferior of rib (costal groove)
chest tube above rib, if below then likely nerve damage
lymphatic drainage in thoracic wall and lungs
clinical relevance
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
Function of Pleural space recesses at the costomedial and diaphragmatic aspects of the lungs
room for lung expansion during inspiration
What side of the lung are you more likely to aspirate into?
Why?
inferior lobe of the right lung
Right is wider and more vertical than Left side
Once the cartilage disappears, the airways are called ______
bronchioles
Describe the full blood supply of the lungs
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.
Sympathetic innervation of Pulmonary
Where do postganglionic fibers come from?
SNS: bronchodilation, vasoconstriction, decreased mucus secretion.
The postganglionic fibers originate in sympathetic chain ganglia in the superior cervical ganglion to the T5 sympathetic ganglion.
Parasympathetic innervation of Pulmonary
What nerve supplies this?
PNS: bronchoconstriction, vasodilation, increased mucus secretion.
vagus nerve
Minute Ventilation
= RR x VT
Respiratory Rate x Tidal Volume
Oxygen Uptake
How would you determine it
Respiratory Quotient
CO2 output/ O2 uptake
R(exchange ratio) is measured; RQ is inferred
determined by the tissues metabolic rate
Gross and Microscopic finding of Diffuse Alveolar Damage (DAD)
Gross: lung is heavy, firm, red-tan appearance
Micro: Hyaline membranes, type II pneumocyte hyperplasia, inflammation microscopically
Idiopathic pulmonary fibrosis (IPF)
What characteristics
Gross
Micro
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
Interstitial (Atypical) pneumonia
- diffuse interstitial infiltrates
- relatively mild upper respiratory symptoms (minimum sputum and low fever); ‘atypical’ presentation
- caused by bacteria or virus
Sarcoidosis
characteristics
- 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.
pneumoconiosis pathophysiology
what ABC’s cause it?
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
Coal Workers Pneumoconiosis
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”
Silicosis Pneumoconioses
pathophysiology
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
Asbestos Pneumoconioses Pathophysiology
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
Why is the peripheral airway considered the ‘silent zone’
what causes more increase in resistance: central or peripheral damage?
peripheral airways (d < 2mm) have a large total cross section w/ many small airways in parallel –> low resistance (20%)
Best type of breathing for Obstructive Disease
Slow, deep tidal volume will result in higher elastic work during breathing (optimal for increased resistance in obstructive disease)
Best type of breathing for restrictive lung diseases
Fast, shallow tidal volume –> higher resistive work during breathing (elastance is increased in restrictive disease)
At high lung volumes, near TLC, where in the lung is resistance high and low?
intraalveolar vessels (high alveolar pressures compress the vessels)
resistance is low extraalveolar vessels, which are distended with blood.
At low lung volumes, near RV, lung resistance is highest and lowest where?
high in the extraalveolar vessels (the vessels collapse)
resistance is low in the intraalveolar vessels (they remain open because alveolar pressure is lower).
At what capacity is pulmonary vascular resistance the lowest?
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.
Alveolar hypoxia does what to the vessels?
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
Obstructive vs. Restrictive airway
FEV1
FEV1/FVC
FEF25-75
How do you diagnose a Pleural Effusion?
- 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)
Difference b/w transudative and exudative pleural effusions
Pathogenesis of Acute Respiratory Distress Syndrome (ARDS)
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
Centriacinar Emphysema
