pulmonary school

pharynx to T10 to the stomach

• pericardium and the left atrium (base of heart)
• vertebral bodies of T5 – T10

proximal 2/3: esophageal arteries which are branches of thoracic artery. Azygous vein/hemizygous veins 

distal 1/3: left gastric artery (branch of celiac trunk)--drained by left gastric vein

esophagus, vagus nerves, thoracic duct also found in the superior mediastinum

• thoracic aorta, azygos vein, and
• hemiazygos vein are ONLY found in the posterior mediastinum

These are important clinically because although normally occurs due to structures that lay around nearby the esophagus-- easy to lodge food, constrictions slow down flow of corrosives, passage of surgical instruments is more difficult

• the aortic arch 
• the esophageal hiatus 
• left main stem bronchus

• o Oblique (aka major)
• o Separates superior lobe from inferior lobe
• o Separates middle lobe from inferior lobe

• o Horizontal (aka minor)
• o Separates superior lobe from middle lobe

Left: cardiac notch and has an oblique fissure separating the inferior and superior lobes

right: oblique (major) and horizontal fissure--inferior superior and middle lobes

directly located on the lung and is not innervated by nerves so insensate

• o Strong fascial tissue layer overlying the apices
• of the lungs

o Provides rigidity to the thoracic inlet

o Provides apical support for the pleural cavity

skeletal muscle innervated by phrenic nerve-- constricts during inspiration--descends to increase thoracic space

all the muscle fibers come together as a central tendon 

• closed-air enters the pleural cavity from damage of lung
• parenchyma and visceral pleura.

• open- hole in the chest wall which allows air to enter
• the pleural cavity.

costodiaphragmatic recess

spaces where the pleural cavity is not occupied by lung tissue

costodiaphragmatic recess is formed by the costal and diaphragmatic pleura--larger of the two recesses.

costomediastinal recess is formed by the costal and mediastinal pleura --left is larger than the right due to the projection of the heart.

posterior pleura extends to the 12th thoracic vertebrae/rib 

right below are the kidneys--so any retroperitoneal procedure can affect the pleura

3 goose and 1 duct 

• vagus nerve
• esophagus
• azygous vein/hemizygous vein 

thoracic duct and posterior mediastinal lymph nodes

clean up the mucus--give saline and dornase Alfa (DNAase) 

and diagnosed by a pilocarpine induced sweat test there should be a lot of Cl- in the sweat

these people are born without vas deferens 

pancreatic insufficiency because the mucus clogs the ducts-- ADEK absorption is poor, more fat in stools so they will float-- because the enzymes are not being released they will accumulate in the pancreas which can cause further damage to cells and cause diabetes 

Bile duct can be clogged.

deletion of F508 which causes a deletion of phenylalanine-- this gene normally codes for ATP gated CL channel which secretes Cl into mucus and resorbs from sweat.. NA will follow CL and H2O will follow Na

you can do an amnio to see how much surfactant there is--

if preterm delivery is suspected- treat mom w/ steroids to a(t) lung development 

postnatally--artificial surfactant

primary ciliary dyskinesia and all the organs being reversed to mirror image--if the organs are not reversed then its only primary ciliary dyskinesia

mutations in dynein and kinesin that render it nonmotile--it can lead to bronchiectasis because increased risk of infection

herniation because of an improperly fused diaphragm--usually left pleuroperiteal membrane does not fuse properly leading to a left sided herniation

fistula--there is a lot of air in the abdomen because of the connection between the stomach and the trachea

too little space: 

Potter's: kidneys in the fetus never develop so they are not able to excrete the amniotic fluid they consume--amniotic fluid decreases--and the baby's face, limbs and chest get compressed 

diaphragm: does not fuse properly--so there is a hole that allows herniation of GI content into thoracic space "flat/scaphoid belly"

• type 1: agenesis: one lung is completely absent
• type 2 aplasia: bronchi is there but the lung is not 
• type 3: hypoplasia the lung and bronchi are bigger on one side vs the other

there are many different kinds: most common is one where the esophagus does not connect to the stomach (so anything they eat will immediately bounce back) but the stomach connects to the trachea 

Chest XR-- will indicate greater air in the stomach 

polyhydramnios-- because the baby is constantly drinking the water and then eventually excreting it--it causes decrease in volume but over here it wont be able to

• capillaries increase 
• gas exchange sites increase 
• tissue density decreases

embryonic period: primary bud creates the main bronchi that give rise to the left and right lung, secondary buds give rise to the different lobular bronchi, third buds give rise to the segmented bronchi--they are all covered in cartilage 

pseudoglandular: bronchioles up to terminal bronchioles (no cartilage) 

• canalicular: respiratory bronchioles and alveolar ducts 
• saccular: terminal sacs that are septated-- surfactant production ***VIABLE BIRTH STARTS HERE WITH GAS EXCHANGE AT 26 WEEKS 

alveolar: increased separation

proliferation of the spanchnic mesoderm creates a septum between the trachea and the esophagus--tracheoesophageal septum--prevents fistula formation 

there is a laryngotracheal groove which is medially established bw the 4th and 6th pharyngeal pouch and the larynx and the trachea will be the first structures to develop 

at 4 weeks: arytenoid swellings push upwards and change the shape of the groove from a slit to a t shape slit (now its called a laryngeal inlet)--epiglottis is located above this

foregut (endoderm)--which will make the respiratory epithelium 

splanchic mesoderm: surrounding smooth muscle, connective tissue and the visceral pleura 

somatic: parietal pleura 

neural crest cells: cartilage 

• childhood: staph aurus 
• adulthood: psuedomonas

• 
• for acute exacerbations: give SABA that act immediately 
• persistent: give LABAS as well they take longer to act but effect is longer acting

Have the patient breathe out, and then as they slowly inhale have the patient squirt the medication...have the patient then hold their breath for a good amount of time

there are individuals who are symptomatic but don't have spirometery changes bc they don't have significant airway obstruction-- in these situations you can do a methycholine challenge where there will be constriction and reduction of FEV

Decreased FEV/FVC if there is airway obstruction, but there are cases of asthma where there isn't an airway obstruction so in this case you wouldn't 

if you have severe obstruction-can lead to air trapping--decreased exhalation causes CO2 buildup which leads to decrease O2 concentration for efficient gas exchange

• 
• over time: in COPD if you do multiple spirometry studies over the course of time they shouldn't be improving (maybe getting worse)

everyone's lung functions eventually go down but more in asthmatics and even more in smokers who are asthmatic-- smoking has a lot of pollutants and allergic inducing factors that cause asthma and if its not properly managed it can lead to COPD

unknown why--based on observation: nasal polyps, asthma, aspirin sensitivity

Cholinergic: Muscarinic receptor 3, causes Ca to be released-- this causes constriction 

Adernergic: stimulates beta receptors which generate CAMP and cause dilation

Antigen presents to dendritic cell and triggers either TH1 (neutrophils) or TH2 (allergic: Il4 (IgE) , Il5 (eosinophils), IL10)-- this inflammation causes smooth muscle and mucus cell hyperplasia (increased amount of cells) and bronchial hyperresponsiveness  (some of the inflammatory agents cause an increased bronchoconstriction response than normal) 

if this is not treated, you get airway remodeling where cells thicken and their protein content changes and so function begins to change. structural and functional changes noted

broncho constriction in response to foreign body and then after a couple days you get mucus plugging 

most people who die from asthma die because of mucus plugging and under treatment

reversible: when you give a bronchodilator to the pt and FEV increases notably 

irreversible: above does not occur (COPD) 

• Asthma-COPD combination: when FEV doesn't rise as much as it does in reversible s/p bronchodilation tx (still noted as irreversible) or give methycholine which normal people don't react to but people with this condition will (FEV will reduce) 

more recurrent in nature

in acute stages it's reversible, but can become irreversible which begins to mimic chronic obstruction disease... there can also be cases that are without obstruction and PFTs are normal

• Perfusion Limited
• • The amount of N2O exiting the lung is limited by the
• rate of pulmonary blood flow 
• • Increased cardiac output increases the total amount of N2O exiting the lung

• Exercise
• • Increased cardiac output causes capillary vasodilation and
• increased blood flow
• • Increased respiration rate increases alveolar ventilation
• • Expansion of the lung increases alveolar volume and thins
• the alveolar-capillary barrier
• • These hemodynamic changes reduce the thickness of the
• gas diffusion barrier and increase the effective surface
• area resulting in an increase in diffusing capacity

you have the person breath in CO (a small quantity) and then have them keep breathing for a couple of cycles

Diffusion capacity= Amount of gas transferred/Palveolar 

Amount of gas transferred= Palveolar (how much gas you were given)- how much gas was in the expired 

should equal 1..anything less indicates diffusion deficit

Cardiac out x (Difference in arterial and venous oxygen content)

age/4

amount of CO2 produced/the amount of oxygen consumed

dust cells (alveolar macrophages)--located within the white space

SPESI determines prognosis which can be used to determine reperfusion intervention of thrombolysis

(in hemodynamically unstable, thrombolytics for sure, you can do catheter based removal but possibility of nicking an artery, surgical embolectomy( if prior two options fail) 

Vena Cava Filters (recurrent despite AC)--Block the path of travel of emboli and prevent them from entering pulmonary circulation.

low to moderate well score and hemodynamically stable (blood pressure is normal): further imaging is determined based on ddimer result 

if high score (BP is normal) --CT angiogram. if contradicted, VQ scan or LE US--start AC right away even before imaging results have come back 

in hemodynamically unstable patients, you can't do any invasive thing--so echocardiogram--diagnosis isn't definitive but justifies additional tx--anticoagulants also started right away- doesnt require imaging results 

• Anticoagulant of choice: 
• Low-molecular-weight heparin (LMWH)
• • Quick to achieve therapeutic target
• • Less incidence of inducing major bleeding
• • Less incidence of heparin-induced thrombocytopenia (HIT)

• • Not a diagnostic test but supportive!
• • Visualize clot in the proximal pulmonary arteries (PE)
• • Presence of clot in the right heart or new right heart strain in a hemodynamically unstable patients with suspected PE wherein echocardiogram may be useful to justify the emergency use of thrombolytic therapy.

Contrast anaphylaxis, pregnancy, renal failure, or CTEPH

• if positive, doesn't mean that you have a DVT/pE
• but if negative, you can for sure rule out the two

BNP and troponin--they determine how hard the right heart is working --and if elevated they indicate a poor prognosis 

• -BNP because fluid backup in the RV 
• -Troponin bc right heart is working harder and may not have the oxygen to compensate

• RV failure due to acute RV pressure overload.
• • Death is due to hemodynamic collapse, not hypoxia.

• lower lobes >upper, and bilateral lung involvement
• originating from DVTS that begin more Proximally--Popliteal, femoral, and iliacs.

because DVT have more blood and are surrounded by more muscle mass and so more likely to break off and travel than superficial ones are

• low blood pressure, decreased heart rate
• venous obstruction 

**varicose veins* are indicative of superficial stasis and can be suggestive of deeper vein thrombosis as well

• protein C deficiency
• protein S deficiency
• hyper-homocysteinemia
• ACLA
• lupus anti-coagulants.

commonly seen in dorm and people living in close proximity with several others 

• causes hemolytic anemia IgM mediated 
• erythema multiforme

seen in farmers and vets-- because zoo animals are most likely to be infected

ticks carry these spores (that are resistant to high temperatures) and it is the only rickettsia organisms because it will cause pneumonia and no skin rash..high Q fevers

atypical virus that is likely to cause interstitial pneumonia and is commonly seen in post transplant immunosuppression or chemotherapy

there is the vagus nerve--cranial nerve 10 which innervates the trachea and the branches of the bronchial tree-- 

• causes bronchoconstriction 
• vasodilation 
• bronchial gland secretion 

Sympathetic is T1-T4 and causes the opposite above

• o The phrenic nerves lie anterior to the roots
• o The vagus nerves lie posterior to the roots

• located inside the trachea. It lies between the right and left
• mainstem bronchi at the level of the sternal angle.

• o Paralysis of half the diaphragm
• o Unilateral injury to the phrenic nerve

• Paralyzed dome:
• o Ascends during inspiration
• o Descends during expiration

• Forced Expiration
• o Internal intercostal muscles
• o Move ribs inferiorly

• o Abdominal muscles
• o Rectus abdominis
• o Internal and external obliques
• o Transverse abdominis

• o Sternocleidomastoid muscles (SCM)
• o Scalenes
• o Pectoralis major and minor
• o Serratus anterior

C6 – T4/5 (sternal angle)

T4/T5 is where the bronchial tree spilts into right and left

• -wider
• -shorter
• -more vertical

left is Anterior to esophagus and thoracic aorta

double layered dead space so the pulmonary veins can expand if there is increased blood flow from that area

left lung--blue is the cardiac notch

Trachea and interpulmonary bronchi: pseudostratified columnar cells with cartilage (the orientation of the cartilage changes) 

**Progressive loss of glands, cilia, and cartilage beyond this point**

• Bronchioles: no cartilage, simple columnar  
• Terminal Bronchioles: simple cuboidal, CLUB CeLLS (have a lot of inclusion type things) 
• respiratory bronchioles: simple cuboidal and squamous

multiple alveoli will dump into it 

• alveolar duct: completely interrupted by alveoli... 
• respiratory bronchioles: slightly interrupted by alveoli 
• terminal bronchioles: are darkly bordered

yellow circle: pulmonary vein: travels in the septi not with any of the bronchi (vein will have less of the darkly rounder stained cells surrounding it like the alveoli do) 

red: the top part is the terminal bronchiole (anywhere where there is dark purple and the vessel looking thing next to it-- blue--pulmonary artery

• A: artery 
• V: venule 
• L; lymphoid tissue (anytime you have small round dots in a region that appears relatively uniform

intrapulmonary bronchi-- the cartilage here is different than in trachea because it is grouped in round vesicles as opposed to a c ring that is connected by the trachealis

semidumes are lined my myoepithelial cells

• Submucosal glands: 
• serous glands: stain darker and release fluidy substance thats rich in proteins 
• mucous glands: stain paler and release more viscous substance that is rich in glycoproteins

• BV is blood vessel 
• P: perichondrium

B are basal cells--the cells that are closest to the basement membrane-- they have regenerative property

• 
• depending on score, you determine whether or not patient will be treated inpatient outpatient or in the ICU

• neutropenia: aspergillus 
• TNF A: fungal and TB
• advanced HIV: pneumocystis

• o Superior: transverse thoracic plane
• o Inferior: diaphragm
• o Lateral: mediastinal part of the parietal pleura
• o Anterior: pericardial sac and diaphragm
• o Posterior: vertebral bodies of T5 – T12