Usmle 1 Pulmonary Physiology

  1. Pulmonary Embryology
    • Notochord develops in the 3rd week of gestation

    • Brain develops in the 8th week of gestation

    • 12th week of gestation the other organ systems begin to form

    • Lung develops in 1st trimester

    • It is derived from the Foregut
    • From the lip → 2nd part of the duodenum, including the respiratory tract = FOREGUT

    • Surfactant is not completely made until 32-34 wks.

    • Lecithin Sphigomyelin ratio is 2:1 to indicate maturity
    •     < 2/1 = ↓ in surfactant → immature
    •        Beclamethasone → (+) surfactant production
    •       If preterm labor w respiratory distress → give synthetic surfactant via endotracheal tube → ↓ mortality
    •     > 2/1 = ↑ in surfactant → enough for labor = mature lungs
    •       Check for Phosphatidylglycerol →breakdown product of surfactant

    • Function
    •     Surfactant acts as an oil
    •     Main job is to decrease surface tension of alveoli → prevents collapse by keeping the alveoli open
    •     If no sufactant → Atelectasis = collapse of the alveoli
  2. Atelectasis
    • Diffusion problem

    • Collapsed alveoli → no oxygen exchange → Respiratory Distress Syndrome = Pulmonary distress in a Premature Baby:

    • When a premature baby is born he goes into respiratory distress until his alveoli pop open.
    •     Need to give baby Oxygen to create a concetnration gradient that will allow Oxygen to get into the lungs.
    •     More O2= more free radical formation → lungs undergo metaplasia and will form a hyalin membrane
  3. Hyaline Membrane Disease
    • Induced by giving O2 to a baby who is hypoxic due to atelectasis.

    • Try to figure blood gasses:

    •  ↓pO2 will cause
    • ↑respiration → ↓pCO2
    • ↑pH

    Restrictive lung disease

    • Need to put baby on a ventilator, PEEP/CPAP
    •     This provides a positive airway pressure to keep the alveoli open → gives some RV
    •  Complicaton: bilateral pneumothorax because of the increased pressure required to infuse the oxygen
    •     Will need chest tube.
    • The free radicals made by oxygen will irritate the airway and stimulates mucous production
    • Goblet cell hyperplasia and hypertrophy
    • Narrow airway lumen = Obstructive lung disease → Bronchopulmonary dysplasia (abnormal growth)
  4. Bronchopulmonary Dysplasia
    • common complication of Hyalin membrane disease

    • obstructive lung disease

    • Acts like asthma

       • Treated the same

    • Majority of children will outgrow O2 by age 2 (when their lungs are almost adult size)

       • Will continue to have obstructive airway disease for the rest of their lives.

    • Artifical surfactant is used to ↓ need for O2 and hospitalization

       • 1st give mother beclamethasone to ↑ baby’s own surgactant production
  5. Adult disease
    • ARDS –

    • • Most common cause
    •    • Sepsis
    •       • Will need intubation and ICU
    •       • Will have same disease course and complications as child
    •       • 60% mortality rate
  6. Aspiration Pneumonia
    • Most commonly involves the Right main stem bronchus & straight down into the right lower lobe

    • If the kid is standing/sitting upright and aspirates, it will go straight down to the superior segment of the R lower lobe

    • If the kid is laying down it will enter the posterior segment of the right lower lobe

    • Only way to aspirate into the upper lobes is to aspirate the foreign body while lying down on their side

        Usually a seizure patient

    • Always look for foreign body in recurrent R upper lobe pneumonia

    • Diagnosis

    • Need to get Inspiratory/expiratory films
    • On inspiration everything inflates
    • On expiration one bronchus remains inflated

    • Removal

    • For a child the best way is to lay them on their stomach and performa back thrust
    • For an adult → Heimliech Manuver
  7. 3 Narrowings of the Trachea where objects get lodged
    • Glottis

    • Middle of the trachea (landmark → aortic arch)

    • Bifuraction of the Trachea at T4

    Image Upload 1
  8. Restrictive and Obstructive pattern
    • MCC of Death → Bronchiectasis

        bronchi are thickened from inflammation and infection

    • Restrictive Disease = problem in the interstitium

    •  O2 diffusion will be affected the most
    •     diffusion and perfusion limited
    •  CO2 diffuses fast so it is airway limited
    •     airway problems, ventilation problems
    • signs of :dyspnea(SOB), and tachypnea(rapid breathing)
    • ↓pO2 ↓pCO2 ↑pH

    • Obstructive Disease = caused by Bacteria producing mucus in Airway

    •  increased respiratory rate of dyspnea and tachypnea
    • normal pO2 ↑pCO2 ↓pH
  9. Amnionic Fluid
    • Function:

    • Create negative pressure around the fetus and absorbs external trauma to the mother’s abdomen
    • In order for the lungs to inflate in the baby you need negative pressure within the amnionic sac.
    • Amnionic fluid is there to keep pressure off of the baby while the negative pressure inflate the lungs

    • Composition

    • 80% is filtrate of mom’s plasma
    • Baby must be able to Swallow & digest → then process → adds 20% to it then urinates in the amniotic sac
  10. Polyhydramnios
    • baby can’t swallow or absorb fluid (neurological, muscular problem, GI obstruction)

    • Mom continues to make 80% of the amniotic fluid but the baby isn’t swallowing it = the baby has a Neuromuscular disease (swallowing is a reflex) or GI obstruction

        Think of Werdnig – Hoffman Syndrome

    • Duodenal or esophageal Atresias can present this way.
  11. Oligohyramnios
    • Low amnionic fluid

    • Baby has renal defect (agenesis/obstruction) and can’t pee → can’t add 20%

    • Will cause increased pressure on the baby because there is no Amnionic fluid to protect the baby from any trauma

    • Potter’s syndrome

    • See the physical manifestation of oligohydramnios
    • ↑atmospheric pressure will cause facial deformity and baby’s facial features to be flattened (due to pressure) = smashed face
  12. Prune Belly
    • No Abdominal wall muscles, therefore can’t bear down to pee, so there is no muscle to push fluid out creating ­ pressure and a prune like appearance in baby

    • This baby will dies of infections (UTI) because always has a catheter
  13. Anatomy of the Lungs
    • Extrathoracic (outside chest cavity) and intrathoracic (inside chest cavity) are separated by glottis.

    • Breath in → Extrathoracic collapses and intrathoracic expands

    • Breath Out → Extrathoracic expands and intrathoracic narrows

    Image Upload 2 Image Upload 3

    • Main stem Bronchus

    • Breaks into parenchyma ½ way and gets smaller

    • After Main stain bronchi will divide into

    • large
    • medium
    • small bronchioles

    • Terminal Bronchiole

    • Most dependent part of airway → therefore, most Lung Cancers like to form here

    • Will deposit in the terminal Respiratory bronchiole

    • Respiratory unit = the only 3 units where O2 Exchange occurs
    •     Resp bronchiole
    •     Alveolus
    •     Alveolar duct
    •         made of 1 layer of epithelium
    •         Can have O2

    • Physiologic Dead Space

    • Composed of all CO2
    • Taking a deep breath can clean out the dead space
  14. Ventilation
    • Total ventilation = ventilation dead space  + ventilation alveolar

    • • TV = VDead Space + VAlveolar 
    • • VMinimum = TV x RR
    •    • Tidal Volume = 10 – 15 cc/kg
    • • Example:
    •    • TV = 600 cc
    •    • RR = 12
    •    • VDS = 40%
    •    • What is the ventilation in the alveoli? Image Upload 4

    • The true measure of ventilation is in the pCO2 changes

    • • If truly ventilating the pCO2 will drop
    • • Patients presenting with SOB/tachypnea are not ventilating properly

    • 500 cc is not universal!!!

    • One can be breathing fast (tachypnic) but not ventilating properly!!!
  15. Chest Cavity
    • Diaphragm normally develops Ventral (midline) → Dorsal (back)

    • Diaphragmatic hernia=

    • Intestines are in thoracic cavity
    • Present with bowel sounds in the chest cavity
    •     See a feeding tube curled into his chest on x-ray
    • Common types:
    •     Bochtalek (90%)
    •         Herniation is in the back
    •  Morgagni (10%)
    •     Herniation is in the front/mid-line
    • Complication
    •     The lung won’t develop because the GI/Intestines are pushing down on the lungs and can’t inflate à pulmonary hypoplasia
    •     Next step is to try and close the hole
    •       Need at least 90% of the lung to develop in order to live.
  16. Lung Histology
    • Trachea :

    • Top 1/3 = Squamous cells (protect against abrasion)
    • Middle 1/3 = Transition cells
    • Lower 1/3 = short colunmnar epitherlium
    •       Beat upward → to swallow foreign debris and let stomach acid digest it

    • Respiratory Epithelium

    • Tall columnar ciliated epithelium (bottom 1/3 and into bronchus)

    • Cilia

    • 9+2 (actin microtubules) configuration =
    • 9 microtubules surrounding 2 actin proteins) Image Upload 5
    • Need a Dynein arm to have flexibility

    • Dynein arm

    • Allow cilia to dissengage from mucus and push it forward to move it always is only one direction → toward the mouth → orad movement
    • When cough, mucus moves 1”/ cough
    • Sinus drainage → short cough
    • Bronchitis → deeper cough...
    • Also needed in sperm
  17. Kartagner’s Syndrome
    • Defect of the Dynein Arm →not working = Can’t clear mucus

    • Triad

    • Obstruction → Bronchiectasis
    • Infertility → because sperm are immotile
    •  Situs inversus (liver/ kidney on other side= midgut rotation)
  18. Common bacteria in the back of the throat
    • Strep Pyogenes

    •S pneumonia - encapsulated

    • H influenza - encapsulated

    • Neisseria Cataralis - encapsulated

    • These bacteria can live in the back of throat because they contain IgA Protease to protect against IgA activity
    • Therefore, they are the MCC of sinusitis, otitis, bronchitis, and pneumonia

    • Cilia prevents these bacteria from entering the lung but if the cilia is paralyzed they can enter

    • Viral infections can paralyze cilia and allow for the encapsulated organisms to come into the lung = SUPER – INFECTION
  19. Cell type
    • Goblet cells:

    • Most numerous
    • serve to produce mucus

    • Type I pneumocytes (95%) –

    • mostly macrophages
    • Found mostly in terminal bronchus where all the dust will settle

    • Type II (5%) pneumocytes

    • produce surfactant
    • Found in alveoli, surrounding alveolar membrane
    • Can become type I, but can’t go the other way round. (Type I can not become Type II

    • Dust/ Clara Cells

    • macrophages that ingest dust particles
    • found in terminal bronchus
  20. Smooth Muscle
    • found throughout airway down to terminal bronchiole

          Can’t have anything in the way of O2 diffusion – so will stop in terminal bronchiole

    • Most abundant in medium size bronchioles

    • Therefore, the most constriction and dilatation occurs here
    • analogous to blood vessels (contain the most β2 receptors)
    • Asthma is a small airway disease but the wheezing is coming from the Medium bronchioles
  21. Cartilage
    • Tracheal and Laryngeal cartilage is of neural crest origin (septum)

    • Trachea has 16-20 C shaped cartilage rings

          Why C-Shape: Opening always faces backwards so esophagus, when full can compress trachea so you are less likely to aspirate.

    • Mid main stem bronchus – start fully circling cartilage

          Because of the lung tissue all around it, if it where not fully encircled it would collapse

    • Stops at the Respiratory unit to allow for diffusion

           Terminal Bronchiole – end of cartilage (because has to be only one layer of cells)
  22. Lung Sounds
    Stridor: narrowing in extrathoracic airway

    • Inspiratory sound only
    • Problem is from Lip to the glottis
    • need a lateral neck film
    • Macroglossia (big tongue) 
    • storage disease 
    • hypothyroidism 
    • Down’s
    • 2nd Brachial Arch problem è microagnathia (small jaw)
    • Pierre-Robin
    • Treacher Collins

    Wheeze: narrowing in intrathoracic airway

    Rhonchi: air moving over mucus

    • Crackles: collapsed airways “popping” open

    • Surfactant is missing
    • Alveoli have been scarred down

    Decreased breath sounds: space between alveolus and chest wall is occupied

    Dullness to percussion: as above

    • Increased fremitus: consolidation on same side or atelectasis on opposite side

    • Bronchophony, egophony, or "ee" to "aa" changes: as above

    • Tracheal deviation: towards atelectasis and away from a pneumothorax

    • Hyperresonance: pneumothorax on same side or atelectasis on opposite side
  23. Lung Infections
    • Croup

    • Bronchiolitis

    • Bronchitis

    • Pneumonia

    • tracheitis
  24. Croup
    • Subglottic edema similar to bronchilitis.

    • Presentation

    • Barking cough and Stridor
    • Steeple sign on neck X-ray

    • Caused by:

    •  Parainfluenze
    • RSV (send to ER immediately)
    •  Adenovirus
    • Influenza

    • Treatment

          Dexamethasone
  25. Bronchiolitis
    • Infectious asthma

    • Includes all symptoms of asthma with acute infection

    • MC in children < 2 years old → can be able to grow out of it

    • Caused by:

    •  Parainfluenze
    • RSV (send to ER immediately)
    •  Adenovirus
    •  Influenza
  26. Bronchitis
    • URI (Upper Respiratory Infection)

    • Acute = ↑ sputem production

    • Chonic = ↑ mucous production for at least 3 consecutive months for 2 consecutive years

    • MCC:

    •  pneumo.
    •  influenza
    •  Catarallis
  27. Airway Infections
    • Epiglotitis: H. Influenza B

    • Tracheitis: C. Diptheria

    • Pneumonia
  28. Epiglotitis
    • closure of trachea

    • Presentation

        Child will be drooling, stridor, muffled voice and fever

    • MCC → H. influenza B

    • Treatment

    • Must make an airway → Intubate in the ER
    •     Look for thumb sign on CXR
  29. Tracheitis
    MCC → Diptheria → EF-2 ribosylation = gray pseudomembrane
  30. Tracheomalacia
    Stridor since birth
  31. Pneumonia
    • Inflammation in the alveolus

    • MCC

    • Strep pneumonia: Rusty colored sputum
    • H flu: Staph Aureus
    •  Neisseria
    •  Klebsiella → currant jelly sputem, homeless alcoholic; likes fissures of lung
    •  Common after flu → S. aureus
    •  Actinomyces → sulfur granules
    • S aureus and pseudomonas → bullae production d/t elastase activity (pneumatocelle)
    • Anaerobic infection – foul smelling; (+) air/fluid levels, gas formation
  32. Interstitial Pneumonias
    • Atypicals

    • Fungus

    • Pneumoconioses

    • Nocardia

    • Sarcoidosis
  33. Atypicals
    • Chlamydia: from 0 to 2 mo

    • Mycoplasma: from 10 to 30 y/o

    • Legionella: over 40 y/o
  34. Fungus
    • Histoplasmosis: midwest

    • Blastomycosis: northeast

    • Coccidiomycosis: southwest

    • Paracoccidiomycosis: South America

    • Aspergillus: moldy hay or moldy basement

    • Sporothrix: rose thorn
  35. Pneumoconioses
    • Asbestosis

    • Silicosis

    • Bissinosis

    • berrylliosis
  36. Nocardia
    the only G+ that is partially acid fast
  37. Sarcoidosis
    • noncaseating granulomas; large hilar adenopathy; high ACE levels
  38. Respiratory Infections (others)
    • Asthma

    • Intrinsic
    • Congenital
    • Cold air/Colds set this off

    • Extrinsic
    • Environmental
    • Offending agents
    • Dust mites >> Roach droppings >> Pet Dander

    • Emphysema

    • Digestion of interstitium by elastase
    • Treat as an OBSTRUCTIVE disease but really is a restrictive disease
  39. Lung Cancers
    • MC intrathoracic = Squamous cell → PTH secretion

    • Small Cell Carcinoma 

    • Anaplastic
    • Located at the carina
    • Produces 4 hormones:
    •     ACTH: 90%
    •     ADH: 5%
    •     PTH: 3%
    •     TSH: 2%

    • MC Primary Lung CA → Bronchogenic Adenocarcinoma

    • Most common lung mass in children is: Hamartoma

    • Most common lung mass in adults is: Granuloma

    Most common TUMOR: adenoma

  40. Physiologic parts to the lung
    • Intrathoracic space

    • Chest wall
    • Pleural space

    • Pulmonary vasculature

    • Pulmonary airway

    Image Upload 6
  41. Lung Volumes
    • RV:

    • Residual volume
    • the amount of air left in the lungs AFTER forced expiration
    • Can not be physiologically forced out
    • Maintains some compliance in the airway
    •  Keeps alveoli from collapsing

    • ERV:

    •  Expiratory reserve volume
    • the amount of air that can still be FORCED out AFTER a normal exhalation
    • Fills up the dead space at rest; decreases the tidal volume that you would have to take in

    • FRC: 

    • functional residual capacity
    •  FRC = RV + ERV

    • TV:

    • Tidal volume
    • the amount of air you take IN during a NORMAL inhalation effort
    • 10 – 15 cc/kg

    • IRV:

    •  inspiratory reserve volume
    •  the amount of air you can FORCE INSPIRE after a normal inhalation effort

    • TLC:

    • Total lung cap
    • ALL the air in your lungs at the END of a deep breath
    • RV + ERV +TV + IRV

    • VC:

    • Volume cap
    • all the air you can breathe in AFTER forced exhalation
    •  ERV + TV + IRV

    • Obstructive Disease

    • RV changes 1st = ↓
    • In both TV changes last

    • Restrictive Disease

    •  VC drops 1st; TLC drops next
    • In both TV changes last
  42. Inspiration
    • Beginning: expansile forces of the CHEST WALL is greater ( 0 to 49%)

    • Middle: expansile forces of the LUNG is greater ( 50 to 99%)

    • End: recoil force of the chest wall EQUALS the expansile force of the lung
  43. Expiration
    • Beginning: recoil forces of the CHEST WALL are greater ( 0 to 49%)

    • Middle: recoil forces of the LUNG are greater ( 50 to 99%)

    • End: the recoil force of the lung EQUALS the expansile force of the chest wall
  44. Breathing in…
    • FRC: baseline > intrathoraxic pressure is negative ( - 3 to – 5)

    • TV: intrathoraxic pressure gets more negative ( -10 to -12)

    • TLC: intrathoraxic pressure most negative (-20 to -25)

    • Intrathoraxic Pressure should always be NEGATIVE
  45. Intrathoraxic Pressure
    • Should ALWAYS remain negative

    • Should decrease with inspiration

    • If it gets positive, then it will resist any blood or air from entering the thorax

    • If you do not breathe in, there will be NO pressure gradient for blood to enter the thorax
  46. Positive Intrathoracic Pressure
    • Kussmaul sign: increased JVD with inspiration

    • Pulsus paradoxicus: exaggerated drop in BP( more than 10mmHg) or pulse ( more than 10bpm) on inspiration

    • Mcc: pericardial tamponade or pneumothorax
  47. Pericardial Tamponade
    • is when fluid in the pericardium builds up

    • if equal pressure on both sides of chest

    • Mcc: trauma or cancer

    • CXR: enlarged cardiac shadow

    • ECHO: compressed small heart

    • Tx: pericardiocentesis

    • If recurrent: put in a pericardial window
  48. Pneumothorax
    • if NOT equal pressure on both sides of chest

    • Traumatic

    • Spontaneous

    • Associated with estrogen use or collagen disease
    • Less than 25% occupation & asymptomatic
    • More than 25% occupation or symptomatic

    • Tx: chest tube placement

    Image Upload 7
  49. Flow ( Q )
    • As you breathe in, the lung Inflates, pulling on traction fibers attached to vessels

    • As vessels DILATE, flow increases

    • As flow increases, oxygen dilates the vessels, significantly increasing Q

    • The increased Q keeps the pulmonary valve open longer, INCREASING S-2 splitting
  50. Flow ( Q ) is greater to the bottom of the lungs because…
    • (1) gravity

    • (2) less resistance

    • (3) more oxygen goes to the bottom of the lungs with each breath

    • Normal RR = 12 to 16 breaths/min

    Q increases on inspiration and decreases on expiration.
  51. S-2 Splitting
    • It is caused when the closure of the aortic valve (A2) and the closure of the pulmonary valve (P2) are not synchronized during inspiration

    • Increases on inspiration due to Increased pulmonary blood flow

    • Decreases on expiration due to decreased pulmonary blood flow

    • This is why RIGHT sided heart sounds increase on INSPIRATION

    • This is why LEFT sided heart sounds increase on EXPIRATION

    Image Upload 8
  52. Oxygenation
    • Directly related to DIFFUSION and PERFUSION

    • More oxygenation is accomplished at the bottom of the lungs only on inspiration

    • Most of oxygenation is accomplished at the top of the lungs > ALWAYS OPEN!
  53. Ventilation (V)
    • Inversely related to pCO-2

    • Definition: patent airway

    • Measurement: pCO-2 ( on ABG’s)

    • More V to the bottom of the lungs only on inspiration

    • Most V at the top of the lungs because it is ALWAYS PATENT
  54. The Law of V / Q
    • V /Q is greatest at the top of the lungs, equally matched in the middle, least at the bottom

    • If you change one, you MUST change the other in the SAME direction

    • ANY V / Q mismatch will lead to hypoxia

    • Eisenmeger Syndrome

    • • Pulmonary HTN that reverses blood flow
    • • Rx:  Nitrous Oxide → dilates pulmonary vessels
  55. Pulmonary Airway Pressure
    • The Only Pressure That Gets Positive With Each Breath

    • Pa = Patm   at IRV and FRC

    • Pa < Patm   at inspiration

    • Pa = Patm   at end of deep breath

    • Pa > Patm   at expiration
  56. Compliance
    • ability to distend and increase volume

    Image Upload 9

    Image Upload 10
  57. V/Q mismatch
    Black = normal

    Red = obstructive leaving air inside

    Blue = emphysema, trouble breathing in and breathing out. (obstruction)

    Image Upload 11
  58. Respiration Bodies
    • Carotid Body

    • • located at the bifurcation of the internal and external carotids
    • • Measures PO2, PCO2, pH, and H+ ions
    • • Afferent (CN IX) and Efferent (CN X)

    • AORTIC BODY

    • • found in the arch of the aorta
    • • Measures pCO-2, pH, and H+ ions
    • • Afferent and Efferent are both CN X
  59. Signals from the lungs and chest wall
    J-receptors: found in the interstitium of lungs

    • • Senses interstitial particles
    • Increases respiratory rate (Tachypnea)

    Slow adapting receptors: found in the ribs,especially the sternocostal junctions

    • • Senses stretch and inflation of ribs
    • • Causes exhalation
  60. Sinuses
    • Maxillary

    • Ethmoid

    • Sphenoidal

    • Frontal

    Image Upload 12
  61. BRAIN IN RESPIRATION
    • More sensitive to elevated pCO-2

    • Hypoxia and Hypercarbia (abnormally elevated CO2) are synergistic

    Image Upload 13

    • Forms of pCO-2:

    • • regulated in pons
    • • 90% in the form of HCO-3 (acid)
    • • ↑HCO3 → metabolic alkalosis → low vol state
    • • ↑pCO2 detected by pneumatic center
    • • if u give O2 it will knock out apneustic center and kill the patient
    • • 7% as carbaminohemoglobin and carboxyhemoglobin
    • • 3% is dissolved ( .03pCO2 )
  62. Pons Components
    • Pneumatic

    • Apneustic

    • Medulla
  63. Medulla
    • Responsible for BASIC functions; has a RR of 8 to 10

    • BRAIN DEAD: no function above the medulla and flat EEG but can still breathe

    • COMATOSE: cerebral cortex is still alive, but patient unable to respond
  64. Apnea
    • Central Apnea: NO inspiratory effort, with or without bradycardia, in 20 seconds or more

    • • Apnea monitor
    • • Tx: Caffiene; theophylline

    • Obstructive Apnea: occlusion of airway during sleep, usually caused by obesity

    • • Snoring will cause R sided hypertrophy and HF
    • • Weight loss
    • • Progesterone
    • • CPAP
    • • Surgery: Uvulopalatoplasty
  65. Pons
    RESPONDS to the environment

    Locked-In syndrome: damage to pons; patient only able to blink as response

    • Most sensitive to osmotic shifts > Central Pontine Demylinolysis

    • Apneustic center: senses hypoxia; causes inspiration

    • Pneumotactic center: senses hypercarbia; causes exhalation (obst lung disease)

    • pCO2 regulator

  66. Kussmaul Breathing
    • RAPID, DEEP breathing

    • ↑pCO2

    • Means METABOLIC ACIDOSIS
  67. Apneustic Breathing
    Pneumotactic center is desensitized, as in COPD

    • A lesion below the pneumotactic center but above the apneustic center
  68. Breathing charts
    Image Upload 14
  69. Cheyne-Stokes Syndrome
    • knock out the medulla

    • Occurs when ↓ glucose and ↓ blood supply

    • Remove ATP from medulla (when hungry)
  70. Thoracic Outlet Syndrome
    • Born with a extra, high cervical rib

    • When the child turns his head the cervical rib will impinge on the subclavian → a vacuum forms and forces blood to stop being shunted to vertebral artery
  71. Subclavian Steal Syndrome
    • atherosclerosis of proximal subclavian

    • Once they raise their arms cut off subclavian artery and pass out

    • Seen in elderly
  72. Obstructive Lung Diseases
    • Bronchitis

    • • Acute
    • • chronic

    • Bronchiolitis

    • Asthma

    • • Intrinsic
    • • extrinsic

    • Cystic fibrosis

    • Bronchiectasis

    • Emphysema

    • • Panacinar
    • • Centroacinar
    • • Distoacinar
    • • Bullous

    • Staph aureus

    • Pseudomonas
Author
docbrito
ID
347927
Card Set
Usmle 1 Pulmonary Physiology
Description
Pulmonary Physiology
Updated