Respiratory - Anatomy and Physiology

*Alveolar Cells

  • type 1 pneumocytes = squamous gas exchange cells
  • type 2 pneumocytes = cuboidal surfactant cells

Type

Blood BB and Tight Junctions

Notes:

  • note that type 2 pneumocytes have the unique ability to proliferate themselves and also be progenitor cells for type 1 pneumocytes
  • type 1 cells make up 95% of the alveoli, where type 2 are only 5% but they are completely necessary for their progenitation of type 1 cells and for the surfactant they make to stop the alveoli from collapsing

Clinical Case

dropped image link

dropped image link

Lung Anatomy

Change of Cells from Trachea --> Bronchi --> bronchioles --> Alveoli

dropped image link

Change of cells as moving towards alveoli

  • cilia important to move things up
  • important for cilia below the mucus making cells
    --> stop mucus accumulation near alveoli

dropped image link

dropped image link

Notes:

  • note that the cilia are the last things to leave as moving distally before the alveoli
    --> make sure no mucus or anything ends up in the alveoli
  • in the alveoli you start to get the type 1 pneumocytes and type 2 pneumocytes
  • type 1 pneumocytes = 90% = squamous cells = gas exchange
  • type 2 pneumocytes = surfactant makers = proginators for type 1 pneumos

Clinical Case

*Hemoglobin

Haldane Effect (in lungs)

  • unloading of CO2 and loading of O2
  • Hb need to deliver H+ protons also to convert bicarb (= primary transporter of CO2)
    --> into CO2 and H2O

dropped image link

dropped image link

dropped image link

Clinical Cases

Clinical Case

Notes:

  • note that

Clinical Case

dropped image link

Bronchioles and Resistance

  • generally decrease exponentially
    --> only exception is initially there is a decrease in SA and slight increase in resistance

dropped image link

dropped image link

*Minute Ventilation / Alveolar ventilation

  • how much air enters the TOTAL respiratory system
    --> includes physiological deadspace

dropped image link

Physiological dead space

  • anatomical + alveolar dead space

dropped image link

*Clinical Anatomy of Lungs

  • 6,8,10, 12 rule for lung markings

dropped image link

dropped image link

dropped image link

*Clinical Symptoms in Respiratory Diseases

  • dyspnea, SOB, pleuritic chest pain

dropped image link

Notes:

  • ONLY the parietal pleura has pain sensation
    --> parietal = PAIN
  • viscera pleura has NO pain sensation
  • note there are 4 separate parietal pleura in the lungs for all the different surface
  • the phrenic nerve gives pain sensation to the diaphragm and mediastinal parts
  • the apices and costal parietal are from the intercostal nerves

*PFTs = Pulmonary Function Tests

dropped image link

COPD PFTs

  • increase

dropped image link

PFTs and *Aging Lungs

  • Total lung capacity stays the same throughout your life
  • calcification of ribs and osteoporosis/increased kyphosis
    --> decreased compliance of chest wall
  • loss of elasticity of lungs
    --> increased compliance of lungs
  • these 2 compliances cancelling each other out
    --> leads to the unchanged TLC
  • elements of both restrictive and obstructive disease
  • obstructive --> alveoli increase in size = air trapping
  • restrictive = FEV1 decreases from restrictive compliance of the chest cavity

dropped image link

dropped image link

Clinical Cases

Clinical Case

Notes:

  • note that

Clinical Case

dropped image link

*Home

*ABGs

  • Arterial Blood Gases

dropped image link

*High Altitude ABGs

  • hypoxemia due to low pressures of O2
  • carotid mecahnoreceptors sense low O2
    --> central resp hyperventilate
    --> expel CO2, still no O2 increase
  • arespiratory alkylosis
  • takes 24 hours for renal compensation of bicarb

dropped image link

dropped image link

Clinical Cases

Clinical Case

Notes:

  • note that

Clinical Case

dropped image link

*Gas Exchange in the Lungs and Alveoli

  • normal O2 arteriole = 100
  • normal CO2 arteriole = 40
    --> note ONLY 45 in veins, not much higher
  • O2 and CO2 are almost the same on their way back through the veins
    --> CO2 is only slightly higher , PCO2 = 45, PO2 = 40

dropped image link

dropped image link

DIffusion vs Perfusion effects on O2 and CO2 in blood

  • under normal circumstances, alveolar walls have quick enough diffusion so that perfusion is the main limiting factor in gas exchange
  • during 1/3 trip through the pulmonary veins, the blood already equilibriates
  • ONLY in 2 cases = exercise and Pulmonary fibrosis/emphysema = when diffusion is the limiting factor
    --> alveolar walls too thick in IPF and COPD
    --> in exercise blood flow is too fast
  • CO2 equilibriates 20 times faster than O2
    --> even in these 2 states, CO2 is NEVER affect, stays the same
    --> when CO2 is equal and O2 is not, = diffusion problem

Clinical Cases

Clinical Case

Notes:

  • note that

Clinical Case

dropped image link

Lung Perfusion, ventilation and *V/Q ratio

  • V/Q ration highest at the apex, lowest at the base
  • effects are mainly due to gravity on the blood = perfusion = Q
  • gravity pulling the lungs alveoli downaward and stretching them
    --> makes them less compliant and can't expand when air enters
  • base is lower and thus gravity --> higher V and Q separately
  • gravity effects blood > lung tissue > air
    --> perfusion = Q up more at the base relative to ventilation = air/lung tissue = V
    --> V/Q goes down at the base

dropped image link

dropped image link

WOB = *Work of Breathing in normal, restrictive, obstructive patients

  • people try to breathe where their WOB is minimized
  • for restrictive lung diseases, they can't take deep breaths since they are restricted
    --> restrictive take many, fast and shallow breaths to minimize WOB
  • obstructive = COPD obstruct the outflow by smaller diameter of bronchioles and lung trapping/turbulence
    --> thus to minimize WOB they want take slow, long deep breaths to minimize WOB

dropped image link

Clinical Cases

Clinical Case

Notes:

  • note that

Clinical Case

dropped image link

dropped image link

Dual *Blood supply to the lungs

  • both the bronchial arteries (O2 rich) and pulmonary veins (CO2 rich)
    --> carry blood to the alveoli
  • they then anastamose after the alveoli
    --> reason for PaO2 drop from alveoli =104 --> 100 in left atrium
  • note also the thebesian veins drain blood from the lungs directly into the left atriuma dn ventricles
    --> another shunt of deoxygenated blood back into the circulation

dropped image link

dropped image link

*Surfactant

  • made and stored in type 2 pneumocytes of the alveoli
  • precursor lethicin
    --> lecithin sphingomyelin (L:S) ratio > 2
  • surfactant stored in lamellar bodies of type 2 cells and are released as buds into the alveoli
    --> from there they break out into the alveoli and eventually recycled back into the type 2 cells
  • 30 wweeks is magic number for L/S ratio >2
    --> premature to this infants at risk for NRDS
    --> collapse of alveoli and lungs = atelectasia

dropped image link

dropped image link

*Flow Volume LOOPS

  • LOOP = means 1 breath tracing of inspiration and expiration
    --> gives more detail of a single breath pattern than a normal PFT
  • slope of FEV1 shows whether COPD vs IPF
    --> COPD has a DIP in the slope of FEV1
  • look at the AMX and MIN of graph for expiration and inspiration
    --> IPF is restricted so has a short graph in both max and min

dropped image link

dropped image link

FEV1 decreases starting at age 30

dropped image link

Smoking effect on FEV1 and cessation of smoking

  • starting at age 30 there is a gradual decline in FEV1
  • smoking accelerates this
  • smoking effects are irreversible, but you can slow the progression if you quit

dropped image link

Clinical Cases

Clinical Case

Notes:

  • note that

Clinical Case

dropped image link

A-a *Gradients

  • check always in initial Mx for dyspnea and SOB
  • rule out PE
  • normal tracheal O2 = 150
  • normal Alveolar O2 = 104
    --> this should match = arterial
    --> thus A-a gradient = 0 normally

dropped image link

*Hypoxia Management Map

  • NORMAL A-a gradient ?
  • RAISED A-a gradient ?

A-a gradient ?

NORMAL A-a gradient

  • rules out PE

RAISED A-a gradient

  • sign of PE
  • V/Q mismatch
  • increase in physioloigcal deadspace

dropped image link

dropped image link

dropped image link

High Tidal volumes (with hypoventilation) are better for efficient breathing

  • rather than hyperventilation = rapid breaths (with low tidal volume)
  • note you need the high tidal volume to fill the lung and get over the gap of anatomical dead space that is always there of the bronchi
    --> this is always 150 of the total 500 that is in the lungs
    --> even in a healthy person

dropped image link

dropped image link