Lecture 8: Obstructive Pulmonary Disease Flashcards
describe conducting airways
we have movement, we breathe in and we need that to go to our respiratory zones for gas exchange to happen
We have movement from conduction to resp zones, but air has to get down to the gas exchange for it to be functional
When pts lightly breathe/hyperventilate/struggle to breathe what happens
not enough gets into our respiratory zones which decreases the oxygen
When people start breathing quickly they do not have effective gas exchange, and CO2 levels increase, O2 decrease
The O2 in our venous blood is not 0 - so we are not using all of our o2 because we have a reserve, but ongoing distress we lose this reserve
Breathing too quickly=not effective gas exchange=increase in Co2 levels and decrease in O2 levels
*slow down their breathing
Body has defence mechanisms- but too much distress won’t help
How do we take majority of meds that help w SOB
we inhale them, so we need to breathe deeply so they get to where they need to be
As we go down to our resp zones it gets smaller and smaller, and if someone is struggling to breathe and takes a puffer then it wont get to our resp zone (where we want it because its more affected down there)
does blood that comes into our heart is it full of O2 or not
Blood that comes into our heart is venous, has lower O2 level and higher CO2 level and goes thru pulm sys and surrounds end zones and in those the concentration (in resp zones) is high O2, low CO2
Generally when our body detects that there is no o2 what happens.
- Brain dilates the vessels to improve perfusion - going to improve o2 delivery
- True in body except in alveoli - because when u have an obstructive condition is there good o2 concentration - but we have trouble breathing out.
- In alveolar it is still returning blood
- Body and lungs say we don’t want there to be blood flow around alveolar because no o2 to exchange with
is pulm sys high or low pressure
Pulmonary sys: low pressure - so when a bunch of vascular beds have constriction - increases the pressure so you now have R side of heart pumping into a higher pressure w can cause R sided HF. This can be a cause of pulmonary HTN.
what does rly advanced COPD sound like
sounds like nothing because there is no air movement
what does COPD sound like
wheezing
what do we want bronchodilation
bronchodilation + reduction of mucous so gas exchange can happen
what is obstructive pulmonary diseases
- most common chronic lung diseases
- include conditions characterized by increased airflow resistance as a result of airway obstruction or narrowing
what is airway obstruction caused by
- accumulation of secretions
- edema
- inflammation of airways
- bronchospasms of smooth muscles
- destruction of lung tissue
- some combination
why is it bad to have trouble breathing out
bc we are trapping stuff in
why is mucus important in the resp tract / why is too much mucus bad
Trouble breathing out - so we are trapping stuff in
Mucosal lining is meant to produce mucus
Normal to produce mucus to line the airway to trap pathogens - irritants result in excess mucous which impacts the ability to have gas exchange
why does asthma occur
- occurs as a result of environmental effects on airways
exposure to allergens or irritants initiates an inflammatory cascade involving multiple cell types, mediators, and chemokines
what happens in asthma
- airway hyperresponsiveness leading to wheezing, breathlessness, chest tightness, and cough
- results in airway inflammation and bronchoconstriction (degree of constriction is related to the degrees of airway inflammation, airway hyperresponsiveness, and exposure to endogenous and exogenous triggers
is asthma reversible
episodic and reversible
what is asthma
thickening of the airway, and secretion/mucous obstruction (thickened airway wall)
Not usually admitted as an adult w this, usually discharged from emerge w inhaler or whatnot, you can also age out of this - don’t know why
what is bronchoconstriction in asthma
relates to responsiveness, exposure, irritant dependent, amount of inflammation (really depends on person, some are rly controlled others an irritant can make it extremely bad)
One of the most common cause of chronic illness in Canada - don’t need to know this though just good to know
describe the early-phase response of asthma
- characterized by congestion
- peak within 30-60 minutes
- vascular congestion
- edema formation
- production of thick, tenacious mucus
- bronchial muscle spasm
- thickening of airway walls
immediate
Doesn’t always progress to the late phase
Take their rescue inhaler and they can mediate that, reduce bronchoconstriction and whatnot but some ppl obviously progress
describe late-phase response for asthma
- primary characteristic is inflammation
- peak 5-12 hours after exposure
- occurs in only 30% to 50% of pts
- can be more severe than early phase and last for 24 hours or longer
Can be prevented
More severe
Going to last longer
- half of ppl w asthma have it poorly controlled
what are risk factors for asthma
- family history of asthma and/or allergy (eczema, allergic rhinitis)
- exposure, in infancy, to high levels of antigen such as house dust mites
- exposure to tobacco smoke or chemical irritants in the workplace
triggers for asthma
- resp infections
- allergens
- exercise/cold
- nose and sinus problems
- drugs and food additives
- gastroesophageal reflux disease
- air pollutants
- emotional stress
why can resp infection be a trigger for asthma
causes increased inflammation in tracheobronchial system
why can allergens be a trigger for asthma
may be seasonal or year-round, depending on exposure to allergen
why can exercise/cold be a trigger for asthma
induced or exacerbated after exercise, characterized by bronchospasm
why can drugs and food additives be a trigger for asthma
sensitivity to aspirin and NSAIDs, β-Adrenergic block (induce bronchospasm), ACE inhibitors (may induce cough), sulfites in food
why can emotional stress be a trigger for asthma
can lead to hyperventilation and hypocapnia, which can cause airway narrowing
is asthma preventable + why dont ppl control it
80% if asthma deaths could be prevented w proper asthma education
- inconsistent practice
- inaccurate assessment of disease severity
- a delay in seeking help
- inadequate medical treatment
- nonadherence to tx
- increase in allergens in the environment
- limited access to health care
- lack of knowledge-pts and HCP
what is included in a asthma assessment
- history/family history
- resp assessment: lung sounds, VS, SaO2, ABG, CBC, lytes
- pulmonary function testing (peak expiratory flow rate, spirometry, forced expiratory volume)
- airway hyper-responsive testing
- chest xray
- allergy assessment
- symptoms over last 2-4 wks
PEFR rate value
400-700 L/min
FEV1/FVC ratio value
0.70
asthma and hyperventilating what happens and what do we prioritize
SNS activation - HR increase, increased bp (due to drop in O2 sat from not getting enough oxygen)
- Treat SOB bc hx
- Prioritize care
- Hyperventilating
○ Can compensate for not deep breathing but this will not last
- Reason why resp distress progresses - it is exhausting! (you are using accessory muscles, SNS activation, etc) so as we move along from normal, to hyperventilate, then it plummets - you have even further compromised bc you have poor exchange AND poor effort
Can put them on ventilator and BIPAP in severe cases, this is when they head to ICU
how does asthma manifest clinically
- unpredictable, episodic, variable
- wheezing - unreliable to gauge severity
- breathlessness
- chest tightness
- cough
- most often at night or early am (2-5)
- expiration prolonged
- onset may be abrupt or gradual
increased signs of hypoxemia
- increased chest tightness and dyspnea
- increased wheezing and coughing
- restlessness
- anxiety
- inappropriate behaviour
- increased pulse and BP
- increased RR
- diff speaking in full sentences
- rescue inhalers are not working
- chest retractions
- cyanosis of lips and skin
- diaphoretic
risk for asthma exacerbation
- asthma exacerbation requiring oral systemic corticosteroids
- poorly controlled asthma
- overuse of SABA
- current smoker
forced vital capacity
blow out forcefully (most should be blown out in the first second)
Never fully empty lungs
75-80% blow out in the first second
categories assessing asthma classification of severity
symptoms
nighttime awakenings
short-acting beta-agonist use for symptom control (not prevention of EIB)
interference w normal activity
lung function
what is the criteria for diagnosis of asthma
- a history of variable resp symptoms
- evidence of variable expiratory airflow limitation
Wheezing, SOB, chest tightness, and cough
(1 or more that are variable in time and length)
*asthma shows improvement
what is the main goals of asthma management
- optimize control of asthma symptoms
- reduce risk of asthma exacerbations
- minimizing medication adverse effects
goals of care for asthma in relation to nighttime awakenings
< or equal to 2 nights per month
goals of care for asthma in relation to meds
< or equal to 2 days per wk for meds for acute relief of asthma symptoms
what are the 3 types of bronchodilators for asthma just state them
- β2-Adrenergic agonists
- anticholinergics
- methylxanthines
what are β2-Adrenergic agonists
- selectively stimulates β2-receptors on airway smooth muscle causing relaxation and bronchodilation
relaxation + bronchodilator
a) SABA:
1-3 min and last 2-6 hours
b) LABA
Larger airways-more air out
Rescue inhaler when you have symptoms
Symptoms all the time-take long term, maintenance meds, everyday
Inhaled corticosteroid is first line of drug
short acting or rescue inhaler (SABA) β2-Adrenergic agonists
this is like our albuterol (salbutamol) (ventolin)
or terbutaline (bricanyl)
- rapid onset: 1-3 min, lasts 2-6 hrs
- taken as needed rather than prescribed daily
long-acting (LABA) β2-Adrenergic agonists
- alternative to higher doses of inhaled corticosteroids
- not used as monotherapy, in combo with ICS
- salmeterol (serevent) - 10-20 mins, formoterol 1-3 mins
- duration of action 8-12 hours
describe to me anticholinergics
inhaled short-acting and long acting
- blocks action of acetylcholine resulting in bronchodilation
- ipratropium bromide (atrovent) - onset 30-60 mins lasts 4-6 hours
- tiotropium bromide (spiriva) - onset 30 min lasts 24 hours
methylxanthines
- dilates muscles around the bronchi
- less effective long term bronchodilator
- alleviates early phases of attacks but has little effect on bronchial hyperresponsiveness
- oral or IV
- narrow margin of safety
- theophylline/aminophylline
not commonly used
3 types of anti-inflammatory drugs for asthma
- corticosteroids
- leukotriene modifiers
- anti IgE antagonists
corticosteroids for asthma what do they do
- suppress inflammatory response
- inhaled form is used in long term control taken on a fixed schedule
- reduce bronchial hyperresponsiveness
- decreases edema in bronchial airways
- decrease mucus production
- control exacerbations and manage persistent asthma
Suppress inflamatory response
Long term control
Acute asthmatic- still give them oral or IV dosing, but long term to maintain asthma or COPD we need inhaled
examples of inhaled corticosteroids for asthma
- fluticasone (flovent)
- budesonide (pulmicort)
- beclomethasone (Qvar), ciclesonide
examples of oral corticosteroids for asthma
methylprednisolone, prednisone
examples of oral/IV corticosteroids for asthma
hydrocortisone, methylprednisolone
leukotriene receptor antagonist (LTRA) for asthma what do they do
- blocks action of leukotrienes - potent bronchoconstrictor and causes increased mucus production
- have both bronchodilator and anti-inflammatory effects
- not indicated for acute attacks
- used for prophylactic and maintenance therapy
- oral
Oral
Not as good as corticosteroids
Not meant for rescue inhaler
They are maintenance!
examples of leukotriene receptor antagonist (LTRA) medications for asthma
montelukast (singulair)
zafirlukast (accolate)
anti-immunoglobulin E antagonists for asthma what do they do
- decreases circulating free IgE
- prevents IgE attachment to mast cells: allergens are prevented from triggering acute allergic reaction
- moderate to severe persistent asthma: control poor despite inhaled steroids
- SQ admin every 2-4 wls
- costly
anti-immunoglobulin E antagonists med example
omalizumab (xolair)
what is the first choice therapy for asthma
corticosteroids!
(reduces inflammation)
budesonide (pumicort) or fluticasone (flovent)
what is the add on therapy to the first choice therapy for asthma
long-acting bronchodilator
(relieves airway constriction)
formoterol (oxeze) and salmeterol (severent)
what is the combination therapy offered for asthma
2 meds in one device yum
symbicort, advair
what are 4 guidelines for meds given for asthma
- asthma drugs are preferably inhaled (need for lower dosage, fewer and less intense adverse effects)
- repeated instruction on how to use the inhaled medication (instruct pt on difference between controller and reliever)
- minimum dose and frequency required to maintain acceptable asthma control
- considered to be safe over many yrs when used appropriately
describe how to give an inhaler w spacer
- remove the plastic cap from inhaler mouthpiece and the spacer mouthpiece
- insert the inhaler mouthpiece into the large opening of the spacer
- hold the spacer and inhaler together and shake well
- forcibly exhale
- put the mouthpiece of the space into your mouth, close your lips around it; do not cover the small slots
- press the metal canister down into the inhaler to spray the medication into the spacer. then breathe in slowly and deeply through your mouth for approx 5 sec
- hold your breath for as long as you comfortably can (approx 10 sec)
- breathe out slowly through your mouth or nose
- if more puffs are prescribed, wait 1 min and then repeat these steps, starting from step 3
DPI vs MDI inhaler advantages
- less manual dexterity is required
- pt does not need to coordinate depressing the canister w inhaling
- an easily visible colour or number system indicates the number of doses left in the device
- no spacer is necessary
DPI vs MDI inhaler disadvantages
- medication may clump if exposed to humidity
- most costly
- require higher inspiratory flow rates
- some contain lactose
- some have shorter expiratory dates
what are soft mist inhalers
- liquid - produces a fine must that moves slowly
- low velocity - 6x more sustained duration than MDI and enhances lung deposition
- delivery is independent of inspiratory flow
status asthmaticus
- severe, life-threatening asthma attack
- refractory to usual treatment
- potentially results in respiratory failure and death
- treatment depends upon severity and response to therapy - severity measured w flow rates
- O2 therapy may be started and monitored w pulse ox or ABGs in severe cases
Severe asthma exacerbation
- Not the same response to atrovent and ventolin (still inflamed and wheezing)
- Can result in resp failure and death
- They are very tired, not breathing effectively
acute asthma episode
- most therapeutic measures are the same as for acute episodes
- increased in frequency and dose of bronchodilators (4-8 puffs q15-20 min)
FEV or PERF below 40% - 1 puff q 30-60 sec (max 20 puffs)
- albuterol/ipratropium bromide
- can be administered via nebulizer - supp O2 is given by mask or nasal cannula for >90-92% O2 sat (ABG monitoring, mech ventilation
- IV corticosteroids are admin every 4-6 hrs, then are given orally. may initially be given orally - pt dependent)
- continuous monitoring of pt is critical - resp assessment
- IV fluids are given bc of insensible loss of fluids
- Ventolin increases HR (tachy)
- Still getting rescue inhalers, but more frequently and higher dosage
- Maybe via nebs if needed
- On an IV or oral steroid + inhaler (at least for a few days to help fight inflammation)
what is green zone for peak flow for asthma
- usually 80-100% of personal best
- remains on meds
what is yellow zone for peak flow for asthma
- usually, 60-80% of personal best
- indicates caution
what is red zone for peak flow for asthma
- 50-60% or less of personal best
- indicates a serious problem
what is COPD
chronic obstructive pulm disease
- airflow limitation not fully reversible
- generally progressive
- abnormal inflammatory response of lungs to noxious particles or gases
(chronic inflammation causes structural changes, small airways narrowing, and destruction of lung parenchyma) - exacerbations and comorbidities contribute to severity
- COPD caused from smoking
- Lungs are compromised, always compromised lung function
- Will always need meds
- Exacerbation-something made it worse
what is the pathophysiology behind COPD
- irreversible airflow limitations during forced exhalation due to loss of elastic recoil
- airflow obstruction due to mucus hypersecretion, mucosal edema, and bronchospasm
- mucus hypersecretion (results in chronic productive cough - not present in all pts)
- dysfunction of cilia
- pulmonary vascular changes
- hyperinflation of lungs (inability to expire air)
- gas exchange abnormalities (resulting in hypoxemia and hypercapnia)
- Hyperinflation of lungs (breathe in a lot, but can’t exhale it all)
- Barrel chest-trapped air
- CO2 retainer, want oxygen level to be less
- CO2 level in blood gradually increases over time
- High CO2 does not inform th body because they are used to it, so their mechanism is low O2 levels
- Give them oxygen, they will lose the drive to breath
2 COPD major subtypes just state them
- chronic bronchitis
- emphysema
what is chronic bronchitis
inflammation and irritation of the bronchial tubes
what is emphysema
damage and destruction of alveoli
what are pulmonary bullae
large air spaces in the parenchyma
what are pulmonary blebs
air spaces adjacent to pleurae
what causes COPD - discuss cig smoking
- stim inflammatory response in lungs
- hyperplasia of mucous glands
- increased production of mucus
- chronic cough
- lost or decreased ciliary activity
how does carbon monoxide cause COPD
decreases O2 carrying capacity
increased HR
impaired psychomotor performance and judgement
how does infection cause COPD
recurring infections impair normal defense mechanisms
COPD heredity causes
α-antitrypsin (AAT) deficiency
how does aging cause COPD
- changes in the lung structure and resp muscles that cause a gradual loss of the elastic recoil in the lung
- lungs become smaller and stiffer
- number of functional alveoli decreases as a result of the loss of alveolar supporting structures
- the thoracic cage become stiff and rigid
COPD diagnosis
- diagnosis is considered w:
- chronic cough
- sputum production
- dyspnea that is: progressive over time, worse w exercise, persistent - recurrent wheeze
- history of exposure to risk factors
- spirometry - post bronchodilator FEV/FVC <0.70
COPD assessment
- history and physical
- resp assessment
- pulm function tests: presence of a post-bronchodilator FEV1/FVC <0.70
- smoking history
- frequency and severity of exacerbations
- serum α1-antitrypsin level
- if indicated: chest x-ray, sputum for gram stain, C&S, ABGs, ECG, exercise testing w oximetry, echocardiogram or cardiac nuclear scan
how does COPD manifest clinically
- develops slowly
- dyspnea usually prompts medical attention: occurs w exertion in early stages, present at rest w advanced disease
- cough, +/- productive
- causes chest breathing (use of accessory muscle, inefficient bc ribs become fixed)
- hyperinflation of lungs/barrel chested
- underweight or overweight
- chronic fatigue, lack of energy
- abnormal lung sounds - wheeze and/or crackles
- late s/s -
1) hypoxemia (PaO2 <60 mmHg or SaO2 <88%)
2) hypercapnia (PaCO2 >45 mmHg)
what are the goals of care for COPD
- prevent
- reduce
- alleviate
- improve
- treat
- improve
- reduce
- end
what occurs when short acting beta agonists and bronchodilators and anticholinergic agents for COPD
together, or alone increased bronchodilation when used in combination
what happens long-acting beta agonist bronchodilators and anticholinergic agents are used to treat COPD + when is this used
- for more severe COPD w persistent symptoms
- LABA (salmeterol and formoterol); anticholinergic (tiotropium) or both
for pts w COPD on inhaled corticoids…what drug is recomended to be added
- monotherapy not recommended
- in combo w LABA - budesonide - formoterol (symbicort), fluticasone-salmeterol (advair)
for pts w COPD on oral PDE4 inhibitors
1. what do we give this for what type of COPD
2. whats the drug example
- COPD w chronic bronchitis
- add on therapy w bronchodilator
- roflumilast
describe COPD nutritional therapy
- 1/3 underwt: loss of muscle mass + cachexia
- high calorie and high protein diet is recommended
- 5-6 small meals/day
- cold foods (produce less sense of fullness)
- less chewing
- decreased gas forming foods
- exercise and treatments 1 hour before and after eating
- fluid intake at least 2-3L/day
describe COPD oxygen therapy-treat hypoxemia
- achieve oxygen sat of 90% or greater
- may be less if pt is a CO2 retainer (SaO2 88-92%)
- low flow or high flow administration
- long term O2 therapy improves; survival, exercise capacity, cognitive performance, sleep in hypoxemic pts
describe COPD pulmonary rehabilitation
walking is best!
describe COPD pursed-lip breathing
prolongs exhalation and prevents bronchiolar collapse and air trapping
describe COPD breathing retraining
- strengthens diaphragm
- decreases dyspnea, improves oxygenation, and slows RR
describe COPD effective coughing main goals
conserve energy, reduce fatigue, facilitate removal of secretions
describe COPD surgical therapy
- volume reduction surgery - reducing the size of the hyperinflated emphysematous lungs, airway obstruction is decreased and room for the remaining normal alveoli to function is increased
- lung transplant
4 COPD complications just state them
- exacerbations of COPD
- cor pulmonale
- acute respiratory failure
- depression/anxiety
describe COPD acute exacerbation (AECOPD)
- sustained worsening of dyspnea, cough, or sputum production that leads to increased use of maintenance meds or supplementation w additional meds
- frequent exacerbations contribute to decreases in lung function and deterioration in quality of life
- increased SOB, fatigue, chest congestion, fever/chills
what do we do for AECOPD
- o2 therapy to treat hypoxemia
- antibiotics (if purulent sputum present)
- increase bronchodilator dosages and frequency of short acting bronchodilators (return to maintenance when pt becomes stable)
- corticosteroids (oral or systemic) like solumedrol or prednisone
- resp support: non-invasive vs invasive
what is Cor Pulmonale for a pt w COPD
- hypertrophy of R side of heart
- w or w/o HF
- result of pulm HTN
- late manifestation of chronic pulmonary heart disease
- eventually causes right-sided HF - dyspnea
- distended neck veins
- hepatomegaly with upper quadrant tenderness
- peripheral edema
- wt gain
describe acute respiratory failure in COPD causes
- exacerbations
- cor pulmonale
- discontinuing bronchodilator or corticosteroid meds
- use of β-adrenergic blockers (should use cardioselective)
- overuse of sedatives, benzodiazepines, and opioids
- surgery or severe, painful illness involving chest or abdomen
describe depression/anxiety for pts w COPD
- 20-50% of COPD pts experience depression
- if pt becomes anxious because of dyspnea, teach pursed-lip breathing
what are the 4 end stage treatments for COPD
- inhaled morphine
- nutritional support
- oxygen
- fans
what is the
1. dose
2. onset of action
3. delivery
4. effect
for inhaled morphine
- 5 mg in 2 mL 0.9% sodium chloride q4h
- approx 30 min, lasting 5-6 hrs
- nebulizer
- decreased dyspnea, calming effect, pain relief
