Upper Resp Tract: nose, mouth, trachea, pharynx
Lower Resp Tract: bronchus, lungs, diaphragm, bronchioles
Alveoli: the very end point of resp tract. On the outside of alveoli is network of capillaries and
that’s how gas exchange happens ~ these two pics are same, but first one highlights how air
flow thru bronchioles into alveoli. And second one shows capillaries outside the alveoli.
Air flows thru bronchioles into alveoli
Capillaries surrounded alveoli
Breathing: inhale air, travels down trachea into bronchus and then into bronchioles and then
into alveoli. Alveoli surrounded by all these capillaries, and this is where gas exchange takes
place. Oxygen we inhale exchange with the Carbon dioxide in the blood, once oxygen is in blood
is binds to HGB on our RBCs and then its taken thru pulmonary vein to the heart and then
oxygen rich blood is pumped out to the body. That’s just ONE breath.
If things don’t work perfectly: obstructive pulmonary disease (obstructive LUNG disease)
Ppl w/ obstructive lung disease has an INCREASE resistance to airflow bc of airway obstruction
like secretions or mucous, OR there is a narrowing in the airway d/t airway swelling.
-they have difficulty exhaling all the air in their lungs bc there is narrowing inside their lungs
-after exhaling, still abnormally amount of air in lungs
Restrictive lung disease: difficult time fulling expanding their lungs with air bc something is
physically restricting their lungs LIKE scoliosis or neuromuscular disease.
-trying to blow up a balloon and balloon is lungs ~ so theres pressure on outside of balloon that
is preventing it from blowing up
Obstructive Lung Disease: trying to blow up balloon but the part im blowing into is super small
so really hard for air to come in and out
Determining whether the problem is issue w outside the lungs or inside the lungs is a critical
piece bc it helps us manage how to solve the problem or relieve symptoms
Obstructive Pulmonary DiseasE:
Common causes: asthma*, COPD*, cystic fibrosis (hereditary disease where body produces
sticky mucous and clogs airway), bronchiectasis (rare and chronic condition where walls of
bronchi are thickened from inflammation and infection
Asthma: affects about 20.4 million adult americans ~ it’s the cause of about 1.7 million ER visits
a year
Incidence: increasing but mortality is decreasing
Gender differences w regard to asthma; more men affected before puberty but more women
affected in adulthood.
-Racial and ethnic disparities as well
-Higher mortality rate in women esp black women
•asthmatic bronchiole:
Asthma is a reversible airflow obstruction cause by inflammation and airway
hyperresponsiveness (bronchospasm) reversible meaning obstruction of lung can generally be
resolved with treatment ~ we can fix it
•inflammation and airway bronchospasm is a problem because alveoli are not perfusing and
ventilating adequately. When the base is smaller , less air is getting in and less oxygen is getting
to our alveoli
•VQ mismatch: V stands are ventilation and Q stands for perfusion for blood flow to the
capillaries
•Normal v/q ration is amount of ventilation coming into lungs is appropriate for blood flow to
the capillary bed
Anything that alters the ventilation or the perfusion is going to the cause the V/Q mismatch.
Case of asthma, our ventilation is not adequate. Mismatch is caused by V: ventilation
Asthma is an inflammation disorder characteristics by combination of bronchial hyperactivity
with reversible expiratory airflow limitation
•caused by trigger which caused inflammation and hyperresponsiveness and then causes
clinical manifestations
Triggers can be related to patients ~ genetic factors (genes can just predispose us from having
asthma and sensitive, can also be related to environment!
Triggers: allergens, exercise, pollutants, respiratory infections ,drug/food sensitivities
, cold weather, occupational exposure, GERD, and psychological factors/stress
Trigger causes inflammatory process in pt and during times of inflammation period,
inflammatory mediators are releases: leukotrienes, etc ~ they cause vasodilation to blood
vessels and nerve cells start itching ~ there is bronchospasm and airway narrowing and then
our goblet cells get triggered to produce extra mucous.
Acid reflux can trigger bronchoconstriction which can set off cascade of inflammatory
mediators
Trigger is psychological factors or stress as well ~ it can worsen symptoms and leave to
hypoventilation and hypocapnia which can lead to real inflammation
Clinical manifestations of asthma: wheezing (air flowing out is harder in the tight space so you
will hear expiratory wheezing~ then progression will be inspiratory and expiratory wheezing, air
is having trouble getting in AND out), coughing, dyspnea, chest tightness, restlessness and
anxiety, increased HR/BP, use of accessory muscles , ABSSENT BREATH SOUNDS ~ EMERGENCY
Stages of asthma:
-early stage: 30-60mins after exposure to triggers
Triggers are sensed and mast cells release the inflammatory mediators
Rest of inflammatory mediators that don’t cause trouble right away so they travel thru blood
stream and recruit reinforcements are eosinophils and they arrive after initial exposures (4
hours after intitial exposure) then LATE stage happens
-late stage: airway inflammation occurs within 4-6 hours after initial attack due to influx and
activation of more inflammatory cells (done by eosinophils) ~ then they degranulate after
coming in contact w airway cells and release their contents and cause even more aggressive
airway inflammation and mucus productions
-occurs in about 50% of pts and symptoms in alte phase can be more severe than the initial
early phase and can last for up to 24hrs or longer
-pts who have acute asthma attack its better to get their symptoms managed and controlled
quickly so that they don’t have a rebound episode of asthma
Since we know that this is what is happening ~ we know how to treat it. Corticosteroids
suppress eosinophils ~ inhaled corticosteroids!!! ~ long term maintenance in asthma
Remodeling: actual structural changes in bronchial wall from airway being chronic inflamed,
happened over long period of time and leads to progressive loss of lung function that is not
fully reversible; results in like a persistent asthma state for the pt.
-development of fibrosis: smooth muscle could get hypertrophied
-muscle or mucous secrete could be hypersecreting
Diagnosing Asthma: based on a combination of factors: history physical, s/s, spirometry and
peak expiratory flow rate
-spirometry: test done that measures movement of air in and out of lungs so when a pt is
scheduled to have this test done. You need to not have pt to take bronchodilators 6-12hours
before test is done*** key component of test bc u want them to do spirometry test initially and
then take bronchodilators again to see if there’s any change of movement**
•Positive to bronchodilator is increased of expiratory rate by 12% more, means asthma can be
reversible
•peak flow meter: helps a pt maintain and keep symptoms at bay by predicting upcoming
attack. Measures peak expiratory flow rate, measures how well air is flowing out of lungs. Peak
flow meter can be done at home or hospital. Asthma pt needs to establish baseline peak flow
rate ~ pt would do this 3xs in a row and then we document each time and then we determine
highest number. Pt needs to do this every day, around same time for 2 weeks period. One
establish highest number for two week period ~ becomes goal to determine what good lung
function. And then you can establish the yellow or red area. Prevents severe symptoms before
it happens. Helps manage symptoms of asthma before they occur. Don’t have to have an order
for this peak flow meter ~ just have a pt use it before and after breathing treatments to see if
theres any change.
Treatment Asthma: based on how asthma is classified; meaning how frequently and severity of
symptoms
-Intermittent, mild persistent, moderate persistent, and severe persistent
•dry powder inhaler: Advair
•metered dose inhaler + spacer if needed
-how to teach someone to use an inhaler
-purpose of spacer is to reduce medication to be deposited directly into mouth
-inhaled medications don’t typically have systemic affects: no sign and symptoms of inhaled
steroid medication vs oral or IV because with inhaled ~ its just going to lunch and working there
as opposed to systemically in body
•IV steroid medication – solu-medrol
•nebulized medication + breathing tubing set up that gets hooked up to compressed oxygen or
air and converts liquid drug med into fine mist so patient can inhale it
•oral steroid medication: if asthma is severe
All asthma med need a quick relief prescribed to them, it is what you pull out first to treat it
-pt who has frequent asthma attacks are on long term medication treatments as well as inhaled
corticosteroids * most effective long term control to treat inflammation *
Pt can develop local effects like thrash, hoarseness and dry cough but can be reduced by using
spacer or having your pt gargle after using inhalation
•Bronchodilators: (albuterol) short acting beta antagonists: stimulates beta2 receptors in
bronchioles to produce bronchodilation (open up), most effective for treating acute
bronchospasm w acute asthma attack. And it relaxes muscle after already tight. Onset happens
within minutes and duration is 4-8 hours. Also prevents release of inflammatory mediators by
mast cells ~ why its told to use this before exercising to prevent upcoming attack
Pt who use quick release bronchodilator to frequently: can feel anxious, palpitations nausea,
tachycardia, tremors . NOT FOR LONG TERM USE: quick relief! (rescure medication)
Long term control: long acting beta agnonists; used once evry 12 hours, hopefully decrease the
need for short acting med. Never used for acute attack. Help long term over time. Large side
effect of beta 2 receptors that short and long term work on is increased heart rate. So beta 2
agonist bronchodilators are designed to bind to beta 2 receptors in lung ~ but it also binds to
other beta 2 receptors and what happens then is that the sympathetic receptors get stimulated
which caused heart go thru period of tachycardia
Inhaled anticholinergics: prevent muscle fiber bands from tightening so they work to decrease
bronchospasm we see that occur in asthma
Corticosteroids: block a late phase response and inhibit migration of inflammatory cells
Oral corticosteroids: long term controlled ~ are used typically for 1-2 weeks for maximum effect
of severe chronic asthma. Prescribed to reduced the bodys inflammatory response after the
asthma attack. You should take oral corticocsteroids for short periods of time to control your
asthma symptoms long term.
Important of adhering to pt management plan. Pt might feel like they don’t have any symptoms
related to asthma so they might not think its important to take long term meds. But we need ot
explain why long term meds are important bc they prevent asthma attack from happening in
the first place. That’s why you need to take them even when youre asymptamoatic
Nursing care related to asthma: encourage health promoting behaviors, teach pt to identify and
avoid known triggers, ambulatory care – teaching regarding drug therapy and monitoring
symptoms, acute care – hospital settings as nurses; monitor resp and cardiovascular systems,
lung sounds before and after breathing treatments ~ establish baseline. Monitor resp rate and
work of breathing, pulse ox and peak flow rates ~ give meds as ordered and evaluate response
to therapy. Decrease anxiety and sense of panic ~ positioning comfortably. Semi-high fowlers to
promote air flow. Pursed lip breathing ~~~ keeps airway open by maintaining positive pressure.
Chronic Obstructive Pulmonary Disease (COPD)
•thick mucus and bronchiole pieces also thickens which make it hard for air flow in and out.
•it’s a aggressive permanent disease characterized by persistent airflow limitation
•COPD is not reversible!! It’s progressive and permanent
•airflow limitations ~ not reversible. Due mainly to loss of elastic recoil. Alveoli aren’t bouncy
and elastic anymore and air flow gets obstructed because mucous edema and bronchospasm so
air gets trapped.
Not all pts with COPD have that sputum and mucous but pretty thick if ur not a secretion
person
•COPD third leading cause of death in US, 16 million americans have COPD.
RISK FACTORS: smoking *** biggest risk factor and development, act of smoking causes
irritation which causes chronic inflammation to the airway., infection is another risk factor (a lot
of recurrent resp infection as a child ~ associated w developing COPD later on as an adult,
ASTHMA another associated risk factor to developing COPD later in life, aging and genetics, air
pollution
•Noxious particles and gasses that someone inhales (tobacco smokes) ~ it causes these four
things in airway : inflammation of central airway, peripheral airway, parenchymal destruction,
and pulmonary vascular changes ~~~~ these 4 things lead to clinical manifestations of COPD
S/S of COPD:
•chronic cough, dyspnea esp w exertion, barrel chest (air entrapment so our lungs are
hyperinflating w air that cant get out eventually lungs hyper expand and causes barrel chest),
sputum production, chest tightness esp w exertion, fatigue (tired from working so hard to
breathe), weight loss (in hypermetabolic state bc they’re working so hard to breathe and
using accessory muscles to get air out), anorexia (bc its hard to eat bc theyre so short of
breath), decreased lung sounds or wheezing, accessory muscle use, edema (sign of right sided
heart failure)
Diagnosis: based on combination of factors: history and physical, spirometry (FEV/FVC <70%)
FVC total volume of air pt can exhale in one breath~~ FEV1 refers to forced expiratory volume
in 1 second, volume of air pt is able to exhale in 1st second~normal can exhale about 70-80% of
breath in that first second so LESS would mean COPD criteria, chest x-ray: not clear diagnostic
tool but it does demonstrate flat diaphragm ~~ there should be a curve to it but if osmoene has
COPD that diaphragm will look flat bc lungs are hyperinflated and are pressing on diaphragm
and flattening it out, ABGs: not purely diagnostic of COPD but monitors progression of COPD for
pts in hospital setting ~~ as it progresses pt will have high levels of carbon dioxide in blood.
Complications of COPD:
Cor pulmonale: pulmonary HTN, pressure inside lungs increased when someone has COPD bc all
the extra air in lungs that cant get out since bronchiole is narrowed and there’s extra secertions
bc alveoli isn’t working well~~ pressure inside lungs gradually increase therefore in order to
push blood in capillary bed surrounding alveoli the right side of heart has to push harder to
push blood into lungs bc lungs have more pressure in them (deoxygenated blood flow thru right
side of heart to the lungs, so eventually right side of heart decides its too tired and takes a little
break and this is when the pt develops right sided heart failure. When right sided heart fails it
leads to extended neck veins (JVD), liver gets bigger (hepatomegaly) due to accumulation of
blood sincfe heart isn’t receiving it in a timely fashion, peripheral edema since blood is
pooling in extremities ~~~ s/s of weight gain (could be a sign of right sided heart failure bc of
this). Acute exacerbation can be a complication for someone that has COPD ~ bacterial and viral
infections can cause acute change in normal breathing pattern cus all the extra mucus ~ ~minor
infections get a lot worst.
COPD management:
-smoking cessation, oxygen therapy, CPAP/BiPAP, lung reduction surgery, lung transplant
Drug management: bronchodilators, inhaled/oral corticosteroids, theophylline,
anticholinergics
•bronchodilators will not reverse s/s like with asthma
•inhaled and oral corticosteroids are used frequently with COPD
•theophylline * specific type of bronchodilator and has a mild anti-inflammatory effect
-monitor for H/A, insomnia, GI distress, and seizures ~~ only therapeutic at a specific range
-blood draws to determine if they’re in a therapeutic range
•anticholinergics work by preventing of bands of muscle around the lungs from tightening.
Bands of muscle help constrict and relax muscle when we breathe, and anticholinergics works
by preventing it
COPD and oxygen administrations:
Oxygen used in long-term therapy for COPD has been shown to alleviate symptoms of SOB and
discomfort of daily activities and exercise ~~ also helps maintain artierla oxygen saturation for
ppl with COPD
•oxygen therapy increases survival and quality of life
•pts are out and about in community with oxygen tank or wheeling it with them
COPD exacerbation ~ getting a resp infection on top of COPD
-oxygen saturations parameters for COPD patients:
Normal: low 90s is threshold for normal patients, 90-91-89, something is wrong. Mid 90 or high
90 level.
-COPD pt: number is lowered, ~ 88% soft number. Bc these patients have a hard time getting air
in and out, so adding oxygen doesn’t always help.
Alveoli doesn’t work that great ~~ a lot of mucus d/t COPD, stretched out, don’t contract well,
bronchiole are also narrowed.
CO2 starts to stay inside ~ COPD patients = CO2 retainers!!
When co2 builds up ~ hypercapnia (body’s pH is decreasing and becoming more acidic)
-kidney starts trying to filter out more acidity but they can’t do it for a long time ~ if Co2 build
up continues ~ they can start getting drowsy and start having neuro problems
Titrating the oxygen to achieve a saturation of somewhere between 88-92% (sweet spot for
COPD pt) we don’t treat the number we treat the patient ~
We want oxygen for body to work but not too much
Respiratory drive theory:
Oxygen toxicity: prolonged exposure to high levels of oxygen resulting in severe inflammation
due to damage that oxygen can cause to the alveoli or capillary membranes.
Leading to; pulmonary edema, shunting of blood (pulmonary alveoli will vasoconstrict which
mean not much blood is going thru capillaries its getting shunt to other places which means
patient has hypoxemia bc not enough blood is moving to the capillaries
Risk of combustion: oxygen supports combustion and increase rate of burning ~ if you are
oxygen at home,
Nonpharmacologic treatments:
Breathing retraining,
Effective coughing
Airway clearance devices
Pulmonary therapy
Chest physiotherapy: postural drainage, percussion
Increase work of breathing ~ decrease use of accessory msucles by using [rused lip breathing ~
someone takes deep breath in and breathe out and pursed lip to allow breath/exhale to last a
longer period of time and more cO2 will be exhaled
•effective coughing referred to huff coughing ~ inhale slowly thru mouth while breathing as
deeply as possible from diaphragm, hold breath for 2-3 seconds and then forceful exhale like
fogging up mirror on window
•airway clearance devices: flutter device, hand held, when pt breathes thru it theres a steel ball
inside that moves up and down
•pulmonary therapy~ rehabilitation therapy: patient or outpatient program for COPD,
exercising training, smoking cessation and nutritional counseling and education, lifestyle
program for someone that has COPD to help maintain highest quality of life quality for them
•chest physiotherapy: ppl that have excessive secretions~~ postural drainage (position pt in
specific way to drain secretions from diff segments of lungs so its easily coughed up),
•percussion: rhythmic cupping that creates hallow sound that fascilates movement of mucus,
typically percuss between towel/sheet or keep gown , vibration helps loosen secretions
COPD nursing interventions:
Patient teaching:
Nutrition: underweight w loss of muscle mass: d/t increased inflammatory mediator response
and increased metabolic rate bc increased resp effort ~~ and lack of appetite cus chronic mouth
breathers and its hard to breathe and eat at the same time. Advice pt to rest 30 mins before
eating and avoid doing strenuous exercise before eating ~~ use bronchodilator prior to meal. Pt
might need supplemental oxygen when they eat
Smoking cessation: COPD is progressive and chronic but when pt cuts back or stops smoking it
can halt the further progression of the disease – if pt shows interest in stopping or cutting back,
let them know it is as positive
Resp Irritants: avoid it ~ avoid pollutant and chemicals
Act. Planning: pts are hesitant to do activities so encourage them to plan activities they can do.
Allow for times of rest.
Psychosocial considerations: pt might feel guilt if they feel like they brought this on themselves
assess for s/s of depression!!! Pt can experience anxiety r/t being in situations where they
might not be able to catch their breath, or forced to do an activity they think they can’t do.
Anxiety provoking situations~
If they can walk up two flights of stairs without difficulty then they’re prob good for sexual
acitivty ~ anyways pt wants to know when they can have their normal life back. Create an
environment where pt knows its ok to ask questions like that.
COPD pts have issues w sleep bc they don’t breathe well at night when theyre lying down so
they wake up tired not really refreshed. Oxygen might eb prescribed at ngiht for them, or they
might benefit from sleeping in a upright position
When to seek medical attention: severe shortness of breath and using their rescure inhaler and
it’s not offer relief ~ seek attention
Chest tightness, chest pains, or disorientation s/s of hypoxia severe so they would need ot seek
medical attention in additional to fever or any s/s of resp infection seek attention
Oxygen delivery:
-nasal canula: accommodate 1-6L of oxygen
-simple mask: 6-12L of oxygen
-nonrebreather mask: reservoir bag that has oxygen in it, so they can just inhale more pure
oxygen and the carbon dioxide gets filtered out and won’t go into bag. They will not
REBREATHE the air they just exhaled.
-BiPAP: bilevel positive airway pressure ventiltory system: noninvasive meaning pt doesn’t need
a tube going into trachea. Tight fitting mask that delivers two diff pressures: bilevel piece of
bipap ~ two diff pressures. Higher pressure when inhaling and lower when pt is exhaling.
Pressure forces alveoli open and allows pt to more easily exhale CO2 that they retained. BiPAP
facilitates more oxygen exchange
-CPAP: continuous positive pressure, only one pressure is provided to pt when inhaling and
exhaling
-high flow nasal canula: tighter fitting, really high levels of oxygen admin – but doesn’t use force
like cpap and bipap machine, it just has two prongs. High flow nasal cannula is humidified~ way
better tolerated than cpap and bipap so someone can theory talk and eat and pt wont feel
claustrophobic. Doesn’t provide that pressure support like the BiPap and CPAp