altered ventilation and diffusion

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mcgpb2592
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183279
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altered ventilation and diffusion
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2012-11-14 10:45:30
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pathophysiology
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patho ch 13
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  1. objectives
    vent/diff roles in o2 and co2 exchange

    processes that can alter v/d

    signs of altered v

    common diagno test and treatment r/t alt vent/diff

    pulm embol, pneumonia, TB, COPD
  2. ventilation
    involves both acquiring o2 (inspiration) and removing co2 (expiration) from the blood

    moving of air

    goal get O2 (need for cell metabolism, remove CO2, pH balance)if porblem can have problems breathing
  3. ventilation is dependant on  (kick drive to breathe)
    a funcitoning respiratory contorl center (brain stem)- control diagphm and lungs

    • lung receptors (2)- periphery-aortic arch- oxygen
    •                                central- right stem- CO2

    * typically measures CO2 can do o2

    chemoreceptors- regular innate, drive to breathe, controlled by CO2 in the body- how body measures how much CO2 is in blood, cerebral spinal fluid is supposed to match it
  4. body wants to get rid of Co2 in the body- central and the other is
    periphery o2
  5. what affects breathing:
    • drugs
    • trauma
    • higher funct: flight or flight incr respiration
    •                      want to hold breaths/ underwater
    • meningitis
    • spinal cord injury
  6. measurements of ventilation: TV, VC, FVC, FEV1, RV, Total lung capacity
    Tidal Volume- volume of air in, out of lungs at rest- norm is 500ml

    vital capacity- max vol of air w/ forced in/exhalation

    forced vol cap- max vol of air w/ forced exhal/ push w/ all might

    forced expiratory vol in 1sec- imp for ppl with asthma

    residual vol- vol of air left in lungs after max expiration

    total lung cap- vol in lungs when max expanded
  7. diffusion
    o2 and co2 are exchanged at alveolar capillary junctions- ACJ

    dependent on partial pressures of co2 and o2 (PaCO2, PaO2), solubility of CO2 and O2, thinness.thickness of the alveolar and capillary membranes
  8. partial pressure in diffusion
    [c] gradient promotes diffusion

    [c] gradient increase co2 level in blood, decr pressure in lungs

    blood pres: arterial blood 80mm Hg and in lungs 40 mm Hg
  9. 2 mj processes occur in DIFFUSION
    • 1. o2 is trying to get to all cells- diffuses quickly
    • 2. co2 is trying to escape the body through the lungs
  10. Sat 02
    can show 100% CO :( 

    shows 100% if has 4 CO's or 4 O2's attached to hemoglobin. 

    not saying that everything is being perfused, not tellling volume stats

    O2 binds to hemoglobin-> iron (important (HbO2))
  11. CO2
    waste product involved in buffering acid-base balance
  12. what is imp for good diffusion
    partial press, surface area, membrane

    *when you sleep you lessen the SA, also lessens SA w/ atelectasis
  13. Ventilation altered by
    • obstruction 
    • suffocation, enlarged tonsils, nasal polyps, asthma, mucus

    inability of neural stimulation & mech of breathing- brain stem 

    drug overdose - toxins-, diaphragm, preg, surgery 

    LEADS TO BLOCKED /INHIBITED AIRFLOW
  14. Diffusion
    exchange of O2, CO2, at ACJ- alveolar capillary junctions
  15. Diffusion is altered by:
    incr thickness of ACJ, decr usable SA of ACJ- emphezma, fibrosis (scarring), infection, edema (fluid, inflamm)

    decr partial press, solubility (high alt, hypothermia, O2 depr)

    *leads to blocked transfer of O2 to circulation and CO2 at atmosphere

    * emph- v and dif problem
  16. alt vent/diff leads to:
    • hypoxemia, hypoxia, hpercapnea
    • then 
    • acidosis
    • then 
    • cell death
  17. partial pressure
    • higher alt--> less O2 more RBC (polycythemia)
    • no good for sickle cell
  18. hypercania
    incr CO2 in blood
  19. hypoxemia
    [c] of arterial O2 in blood
  20. hypoxia
    low oxygen in tissue, causes you to breathe more.

    carbon dioxide is coming out and decr acidity
  21. acidosis
    • high CO2
    • blood is more acidic,

    less Co2- bloos is more basic/alkaline- Alkalosis


    • *metabolic or respiratory related to were problem existed, problem in lungs its respiratory
    • not in lungs-metabolic
  22. V-Q mismatch
    V- air going through alveoli; obsturction, asthma, COPD, emphysema

    Q- amt of blood perfusing through capillaries, 

    normal is .8

    • *vent problem: lung porblem low v below .8
    • * perfusion problem-  (pulm emb.) low q- greater than .8
  23. General Manifestation of impaired Vent/Diff: Cough
    acute cough- resolves in 2-3 wks, underlying cause

    chronic cough- greater than 3 wks (smokers, asthma, pts w/ meds w/ side effects of ACE inhibitors, GERD)

    wet/dry cough

    mucus: color/consistency (TB, bacterial (dark rusty) viral (yellow) staph infection (green))

    hemoptysis: bloody sputum
  24. General Manifestation of impaired Vent/Diff: breathing
    dyspnea: subjective sensation of uncomfortable breathing/ trouble breathing

    orthopnea: stature/position chnage to breathe, dyspnea when a person is lying down

    paroxsymal nocturnal of dyspnea- trouble breathing at night

    pursed lip breahing- prevents SOB, easier way to breathe if you have SOB
  25. General Manifestation of impaired Vent/Diff: lung sounds
    • adventitous:
    • crackles/rales: i/e, hair, fluid, high pitch
    • ronchi: low pitch, mucus
    • stridoe- high pitch, upper airway obstr, trachea
    • dim breathing- obstruciton
    • absent- no air mvmt
    • wheezing- high pitch, airflow obstruc
  26. General Manifestation of impaired Vent/Diff: others
    accessory muscles: abd, diaphragm

    chest pain

    barrel chest:lungs hyper inflate, COPD
  27. General Manifestation of impaired Vent/Diff: breathing 1.2
    changes in breathing pattern:

    Kussamaul respiraiton- hyperpnea- incr vent rate, no expiratory pause.     Ketoacidosis compensates metobolic acidocis 

    Cheyne-Stokes respirations- when there is condition that slows blood flow to brain stem, helps regulate breathing, HR, and autonomic reflexes

    *neuro issue
  28. Lab and diagnostic tests  for impaired vent/diff
    hx, phys exam

    visualization (bronchoscopy, x ray, CT, MRI)

    FEV1

    SaO2- pulse oximetry

    lab studies- cult/sensitivity (tells wt bacteria and what med to use)

    arterial blood gas
  29. Treating impaired vent/ diff
    remove obstr- Touch, Cough, Drug, Breathe, Hydrate

    restore integrity

    decr inflamm/mucus

    supplemental O2, mech vent- but be careful if pt is COPD
  30. Pulmonary Embolism
    • - occulsion of a portion of the pulmonary vascular bed by a thombus, embolus, tissue fragment, lipids or an air bubble
    • - blocks oxygen!
    • - can arise from DVT
    • - sitting still on airplane flights

    virchow triad- venous statis (blood is no longer moving), hyper-coagulability, and injuries to the endothelial cells that line the vessels<----impaires circulation

    depends on the size, where! its caught

    pt breathes heavy, clear lung sounds, not oxygenating, have low pulse o2, but hear lung sounds- TREAT QUICKLY
  31. Pulm Embolism- clin man
    • tachycardia, feeling of impending doom, massive hemoptysis, 
    • SOB, low o2 sat
    • chest pain
    • weak pulse
  32. Pulm Embol
    treat: SCDs, anticoagulants, ted hose, 

    heparin, lovenox, blood thinners
  33. Pneumonia
    • infectious process
    • community acquired pneumonia- streptococcus pn

    nosocomial pheumonia- where you get the bacterial will tell you what antibiotic to use

    pheumococcal pneumonia- can prevent w/ vaccine!

    viral pn- lead to bacterial pneumonia, viral irrate can cause cell death and beteria will have easier time causing infect

    create fluids in lungs, cough up!, inflammation in lungs 

    need to kill bacteria or death or lack of airway clearance

    can lead to alveolar collapse
  34. Pneumonia- patho
    aspiration of oro-pharyngeal secretion

    inhalations via sneezing, coughing, talking, or infected respiratiory therapy equipment
  35. Patho- clin manif
    fever, chills, productive cough, or dry cough, pleural pain, or somethimes hemoptysis

    crackles in lungs- bc of fluids

    too much Co2- periphery issue
  36. Pneumonia- diagno criteria
    CBC- bands, WBC

    chest xrays- see consolidation

    • thoracis ct scan- only if severe 
    • sens/cult  test or gram stain test- antibiotics
  37. Pneumonia- Treatment
    bacterial pneumonia: antibiotics

    adequate hydration and good pulmonary hygiene

    cough up, exspector drugs

    supplemental o2

    * in elderly incr death rate
  38. TB- patho
    mycobacterium tb

    - airborne droplet nuclei tracel directly to terminal bronchioles and alveoli of lung

    can go into remission

    TB bacteria does not do most of the damage instead it is the sustained hypersensitivy 4 reaciton that causes damage
  39. TB- patho- inflamm/immure responses
    containment- asymptomatic, tb not causing problems

    multiplication- progressive TB

    dormancy- can get secondary TB

    * granulomas can form- body cant destroy- wall it off instead and when reactivated then get "coughy" again
  40. TB-and the body
    can attack the liver

    granulomas take up space needed for diffusion
  41. TB- clin manif
    night sweats

    some won't know until they get a chest x ray

    anorexia
  42. TB- diag criteria
    TB skin test

    sputum culture

    chest x ray
  43. TB- treatment
    multi drug regiment

    directly observed therapy (DOT)- come in to take med

    Rifampin, pyra.., INH<- are meds

    placed in isolation
  44. Chronic Obstructive Lung Disease-  airways obstr that is worse with expiration
    problem with vq mismatch

    • common s/s: wheexing, dyspnea
    • causes: smoking- so STOP

    • Asthma
    • COPD- 
    • emphysema
    • chronic bronchitis

    Chr bron and emph- usually occur together! only diff is how you classify them
  45. Asthma- patho/causes
    • mast cell degeneration- produces histamines> inflam complex, neutrophils come in
    • - gums up lungs bc too many secretions!
    • feedback mech- interlelukins and IgE's- more inflamm

    stop quickly! inner city children mostly have

    genetic disorder+ environ= worse issue

    prevent allergic reactiont to prevent cascade
  46. Asthma patho/causes
    once we get cellular inflammation and vasolidation (RBC dilate to take in more o2) and incr permeadbilty you get bronchospasm- constriction of mj airways; air gets trapped; not enough o2; new air cannot come in and ait cannot get out of lungs
  47. Beta blockers
    work in lungs, pt who has asthma and they have beta blockers that target beta 2 make asthma worse.

    anything that is selective for type 2 beta receptors can cause an asthma attack
  48. two types of beta blockers
    beta 1-  selective for just beta 1, can give to asthma pt.  not first time to give to pt, but you can give to pt

    beta 2- not selective; affect beta1 and 2, do not give to asthma pt's.  
  49. Asthma- clin manif
    chronic reactive airway disorder that can present as an acute attack.

    bronchospasms and mucus secretions

    • triggers! inhalant
    • bronchial tubes tighten...this narrow the air passage and interrupts the normal air flow..mucus are plugs
  50. asthma - early phase
    • chest constription, expiratory wheezing, non-productive cough, 
    • more likley to get cold
  51. asthma- severe attack
     use of accessory muscles

    wheezing on both I/E

    • pulsus paradoxus- breathing in (incr blood pressure) force air in lung; normal blood pressure decreases in inspiration
    • - abnormally lg decr in syst blood press 



    status asthmaticus- worse form of asthma- need to intubate, air cannot go in and out of lungs

    asthma in young pts- dont take mes- harder to control 
  52. COPD- Chronic Bronchitis
    its a cold in the lungs

    cough- purulent sputum

    hypersecretion of mucus and chornic productive cough that lasts for @ least 3 mo's and for 2 consecutive yrs

    *obstruction of airflow caused by mucus

    smoking, inhaled, cilia not strong enough to clear secretions, 

    air goes in but has trouble going out bc of secretions blocking 

    • Chronically Inspired irritants
    •  incr mucus production and the size and # of mucus glands, mucus is thicker than normal

    Pulmonary HTN continues and right verntricular end diastolic pressure increases (leads to rt ventricular hypertrophy and rt sided heart failure)


    v/q imbalances results from resistance in small airways and decr arterial oygenation.  hypoventilate bc of a decr respiratory drive

    has clubbing!
  53. emphysema - patho
    told apart from chronic bronchitis from CT scans!!!!

    hacking dry cough 

    • abnormal permanent enlargement of the gas exchange airways accompanied by the destruction of alveolar walls w/o obvious fibrosis
    • leads to tissue changes rather than mucus production

    distinct characteristic...airflow limitation caused by a lack of elastic recoil in the lungs. 


    *when you get this in combo w/ chronic bronchitis you get tiny airways. ppl dont ahve normal o2 sat

    * can have o2 at home, keep it low- if its too high, will lose the drive to breathe, doesnt get co2 out!

    body becomes used to lower o2 rate

    look for dyspnea on exertion...barrel shaped chest form over distention, accessory muscles and abdominal muscle use.
  54. emphsy- diag crit
    chest x ray- air is black 
  55. COPD- patho
    • toacco or other pollutants inflame the lungs
    • chronic inflamm causes remodeling
    • remodeling not helpful w/ mucus production creates dead air space
    • only ends up w/ portion of the lungs that are usable

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