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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
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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
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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
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body wants to get rid of Co2 in the body- central and the other is
periphery o2
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what affects breathing:
- drugs
- trauma
- higher funct: flight or flight incr respiration
- want to hold breaths/ underwater
- meningitis
- spinal cord injury
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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
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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
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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
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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
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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))
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CO2
waste product involved in buffering acid-base balance
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what is imp for good diffusion
partial press, surface area, membrane
*when you sleep you lessen the SA, also lessens SA w/ atelectasis
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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
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Diffusion
exchange of O2, CO2, at ACJ- alveolar capillary junctions
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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
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alt vent/diff leads to:
- hypoxemia, hypoxia, hpercapnea
- then
- acidosis
- then
- cell death
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partial pressure
- higher alt--> less O2 more RBC (polycythemia)
- no good for sickle cell
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hypercania
incr CO2 in blood
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hypoxemia
[c] of arterial O2 in blood
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hypoxia
low oxygen in tissue, causes you to breathe more.
carbon dioxide is coming out and decr acidity
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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
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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
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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
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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
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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
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General Manifestation of impaired Vent/Diff: others
accessory muscles: abd, diaphragm
chest pain
barrel chest:lungs hyper inflate, COPD
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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
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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
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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
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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
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Pulm Embolism- clin man
- tachycardia, feeling of impending doom, massive hemoptysis,
- SOB, low o2 sat
- chest pain
- weak pulse
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Pulm Embol
treat: SCDs, anticoagulants, ted hose,
heparin, lovenox, blood thinners
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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
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Pneumonia- patho
aspiration of oro-pharyngeal secretion
inhalations via sneezing, coughing, talking, or infected respiratiory therapy equipment
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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
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Pneumonia- diagno criteria
CBC- bands, WBC
chest xrays- see consolidation
- thoracis ct scan- only if severe
- sens/cult test or gram stain test- antibiotics
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Pneumonia- Treatment
bacterial pneumonia: antibiotics
adequate hydration and good pulmonary hygiene
cough up, exspector drugs
supplemental o2
* in elderly incr death rate
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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
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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
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TB-and the body
can attack the liver
granulomas take up space needed for diffusion
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TB- clin manif
night sweats
some won't know until they get a chest x ray
anorexia
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TB- diag criteria
TB skin test
sputum culture
chest x ray
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TB- treatment
multi drug regiment
directly observed therapy (DOT)- come in to take med
Rifampin, pyra.., INH<- are meds
placed in isolation
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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
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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
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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
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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
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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.
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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
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asthma - early phase
- chest constription, expiratory wheezing, non-productive cough,
- more likley to get cold
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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
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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!
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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.
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emphsy- diag crit
chest x ray- air is black
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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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