Pulmo. COPD Flashcards
Emphysema. ,,pink puffer”
.
Emphysema. CO2, O2, cyanosis?
CO2 retention
No change in oxygen –> No cyanosis
Emphysema. AP diameter?
increased
Emphysema. exhalation?
prolonged
Emphysema. what characteristic breathing?
through pursed lips
Emphysema. what type in smoking?
Centriacinar
Emphysema. what type in A1AT deficiency?
Panacinar (lower lobes)
Emphysema. A1AT. liver disease associated.
.
Emphysema. A1AT. 4 characteristic?
● COPD at a young age (</=45 years).
● COPD with minimal or no smoking history.
● Basilar-predominant COPD.
● History of unexplained liver disease.
Emphysema. xray?
narrow heart shadow, flat diaphragm, decreased vascular markings and hyperinflated lungs.
inc. AP diameter
Chronic bronchitis. ,,blue bloaters”
.
Chronic bronchitis. definition?
Productive cough for 3 or more months over 2 consecutive years.
Chronic bronchitis. O2?
Decreased oxygen –> cyanosis.
Chronic bronchitis. heart dysfunction?
Pulmonary HTN
CHF
edema
Chronic bronchitis. xray?
CXR: prominent bronchovascular markings and a mildly flattened diaphragm.
COPD and chronic bronchitis most of the time is in combination.
.
hyperinflation. static mechanism.
Static mechanisms: equilibrium between negative pressure of chest wall and positive pressure by the lungs at the FRC. Decreased elasticity of the lungs decreases the positive pressure created by the lungs to expel air. Thus, decreasing the negative pressure created by the chest wall. FRC is reached at a higher lung volume (higher FRC).
hyperinflation. dynamic mechanism.
Dynamic mechanisms: “air stacking”. Increased airway resistance leading to
prolonged expiratory phase. When exertional demands trigger an increase in minute ventilation, the patient is forced to begin inhalation prior to completion of exhalation –> further air trapping and hyperinflation.
Hyperinflation.
diaphragmatic flattening in COPD.
In COPD, the diaphragmatic flattening and muscular shortening caused by
hyperinflation result in more difficulty in decreasing intrathoracic pressure
during expiration and therefore increases work of breathing.
COPD. pulmonary tests.
4?
PFT, DLCO, A1AT, ABG
COPD. PFT? 2
Decreased FEV1/FVC ration
Not reversibel
COPD. DLCO?
DLCO decreased in emphysema, normal in chronic bronchitis
COPD. A1AT?
Tiesiog measue serum AAT levels
COPD. ABG?
chronic respiratory acidosis and secondary metabolic alkalosis.
▪ Vs CHF exacerbation: respiratory alkalosis.
COPD. treatment. medication groups?
Treatment: add more medications if condition is getting worse.
o SABA.
o Add LAMA.
o Add LABA.
o Add ICS.
o Add PDE4 inhibitors.
o Add oral corticosteroids.
COPD. treatment mneumonic - COPDER
Corticosteroids, oxygen, prevention, dilators, experimental, rehabilitation
COPD. treatment mneumonic - C? what effect?
Corticosteroids: decreases COPD exacerbations and improves quality of life.
COPD. Mild - what corticosteroids?
ICS
COPD. severe - what corticosteroids?
Oral CS
COPD. exacerbation - what corticosteroids?
IV CS
COPD. mneumonic - O. What Spo2, what pO2?
SpO2 is less than 88%.
o Keep it between 88 and 92 since they’re dependent on hypoxic drive to ventilate.
● Or PaO2 is less than 55.
COPD. mneumonic - O. Long term supplemental oxygen has mortality benefit with significant hypoxemia.
What SpO2 or pO2?
SpO2</= 88% or PaO2 <55 mmHg.
COPD. mneumonic - O. Long term supplemental oxygen has mortality benefit with significant hypoxemia.
What SpO2 or pO2 with cor pulmonale or RHF or erythrocitosis (>55 proc.)?
SpO2</=89% or PaO2 <59 mmHg with cor pulmonale or RHF or erythrocytosis (>55%)).
COPD. mneumonic - O. Long term supplemental oxygen has mortality benefit with significant hypoxemia. SpO2 maintai above 90proc. when?
SaO2 should be maintained above 90% during sleep, walk, and at rest.
COPD. mneumonic - O. Long term supplemental oxygen has mortality benefit with significant hypoxemia. how long to use to get benefit?
Survival benefits are significant when used for 15 hours or more.
COPD. mneumonic - O. why not above 92 proc?
Why not above 92? ((The hypercapnia would lead to cerebral vasodilation –> may induce seizures.))
oxygen induced CO2 retention in COPD schema atspausdinti
.
oxygen induced CO2 retention in COPD.
Baseline: decr. ventilation,
decr. gas exchange (hypoxic vasoconstriction) –> what after O2 –> what effect?
post O2: vasodilation –> effect: ventilation/perfusion mismatch
oxygen induced CO2 retention in COPD.
Baseline: decr. PaO –> incr. CO2 affinity (Haldane effect) –> what after O2 –> what effect?
after O2: Incr. PaO2 –> decr. CO2 affinity –> Effect: Decr. CO2 uptake from tissues
oxygen induced CO2 retention in COPD.
Baseline: rapid, shallow breathing (incr. RR) –> what after O2 –> what effect?
after O2: decr. RR –> effect: decr. minute ventilation
COPD. mneumonic - P. 2 aspects?
- smoking cessation - decrease the rate of decline of FEV1 and decrease mortality
- vaccines: flu and pneumococcal
COPD. mneumonic - D. 3 drugs in general?
Short acting, long acting, and orals.
COPD. mneumonic - ER
E - experimental
R- rehabilitation
nieko nebuvo prirasyta prie situ.
.
COPD. Rofumilast - ?
Rofumilast: PDE inhibitor that decreases mucociliary malfunction and pulmonary remodeling; reduces future exacerbation.
COPD in A1AT. what specific treatment?
A1AT: IV supplementation with pooled human AAT + bronchodilators + steroids.
▪ Lung & liver transplant if needed.
COPD. to improve survival? 3
o Smoking cessation.
o LTOT.
o Lung reduction surgery.
COPD - progressive condition of limited airflow during expiration that is not entirely reversible.
Encompasses chronic bronchitis and emphysema
.
COPD most important risk factor?
smoking
COPD compliance and elasticity?
loss of elasticity, increase compliance
COPD. features? symptoms
a. Progressive dyspnea
b. Cough with sputum production
c. decr. breath sounds
d. Prolonged expiratory phase
e. Barrel-shaped chest (due to air trapping and hyperinflation of lungs)
f. Elongated and narrow heart shadow on X-ray
g. Chronic hypoxemia may be seen in advanced disease, which leads to secondary polycythemia.
COPD. Hyperinflation in COPD - It occurs through both static and dynamic mechanisms.
.
COPD. air stacking phenomenon?
a. It is the dynamic mechanism for hyperinflation in COPD
b. It is more responsible for hyperinflation than static mechanism
COPD. air stacking phenomenon. pathophysiology?
The expiratory phase is prolonged in COPD
When exertional demands trigger an increase in minute ventilation, the patient is forced to begin inhalation prior to completion of exhalation
This results in additional air trapping and hyperinflation
most important factor for prolonged survival in COPD?
Abstinence from smoking (most important)
(NOT long term O2 or lung reduction surgery)
COPD treatment. what inhaled bronchodilators?
Inhaled bronchodilators (especially anti-cholinergics medications like ipratropium and
tiotropium)
COPD treatment. what combination of drugs?
Anti-cholinergics may be combined with short-acting beta agonists (eg, albuterol)
COPD treatment. for severe COPD drug?
Inhaled steroids and long-acting beta agonists
chronic vs acute-on-chronic COPD.
what metabolic change in chronic? apie hypercarbia
In chronic COPD, there is hypercarbia with normal pH and high serum bicarbonate
chronic vs acute-on-chronic COPD.
what metabolic change in acute-on-chronic COPD? apie hypercarbia
In acute-on-chronic COPD, there is hypercarbia with associated acidosis and low bicarbonate level
This is because of mixed-acid base disorder
selection of bronchod. for stable COPD. Lentele buvo, bbz ten vapsie.
Lower symptom severity + lower disease risk?
SABA or SAMA as needed
selection of bronchod. for stable COPD.
Higher symptom severity + lower disease risk?
LAMA
selection of bronchod. for stable COPD.
Lower symptom severity + higher disease risk?
LAMA +/- LABA
selection of bronchod. for stable COPD.
Higher symptom severity + higher disease risk.
LAMA +/- LABA +/- ICS
selection of bronchod. for stable COPD.
Kas skaitosi disease risk?
In general: Based on frequency of exacerbations
selection of bronchod. for stable COPD.
Kas skaitosi [higher symptom severity]?
Dyspnea with neutral exertion (light housework) or at rest. Assessed using validated instruments, such COPD assessment test (CAT)
nu mazdaug impact of respiratory symptoms in daily life
selection of bronchod. for stable COPD.
Kas skaitosi lower disease risk?
No hospitalization
AND
<2 outpatient exacerbations requiring systemic corticoisteroids
selection of bronchod. for stable COPD.
Kas skaitosi higher disease risk?
> = 1 hospitalization
OR
=2 outpatient exacerbations requiring systemic corticoisteroids
LAMA’s are always superior to LABA’s in COPD
.
COPD exacerbation.
most common trigger?
upper respiratory infection
COPD exacerbation.
characterized by symptoms?
- It is characterized by change in >=1 of the following cardinal symptoms:
a. COUGHT severity or frequency (increased frequency or severity)
b. Volume or character of SPUTUM production (change in color or volume)
c. Level of DYSPNEA (increased)
COPD exacerbation.
physical examination?
a. Wheezing
b. Tachypnea
c. Prolonged expiration
d. Use of accessory respiratory muscles
e. Jugular venous distension is observed, especially during expiration, due to increased intrathoracic pressure
f. Distal heart sounds may be heard due to hyperinflation of lungs
COPD exacerbation.
Diagnosis - xray ->?
hyperinflation
COPD exacerbation.
treatment. initial? 3
a. Initial intervention:
i. SABA
ii. Systemic glucocorticoids (inhaled glucocorticoid have no role in management of COPD exacerbation)
iii. Antibiotics
COPD exacerbation. ABG?
hypoxia, CO2 retention (chronic and/or acute)
COPD exacerbation. persistent symptoms even after initial intervention? what to do
Noninvasive positive pressure ventilation (NPPV)
COPD exacerbation. when need intubation?
i. Failure of 2-hour trial of NPPV
ii. pH <7.1
iii. Hemodynamic instability
iv. Poor mental status (eg, somnolence, lack of cooperation, inability to clear secretions)
COPD exacerbation. prevention. what drug?
Roflumilast
COPD exacerbation. prevention. Roflumilast. mechanism?
It is a phosphodiesterase inhibitor with anti-inflammatory properties
COPD exacerbation. prevention. Roflumilast. action 2?
decr. mucociliary malfunction
decr. pulmonary remodeling
COPD exacerbation. prevention. Roflumilast. use? 2
- It is useful as maintenance therapy to reduce future exacerbations in patients with severe COPD and history of exacerbations
- It is not indicated during an acute exacerbation
COPD exacerbation. management is lenteles?
oxygen
inhaled bronchodilators
systemic glucocorticoids
antibiotics if >=2 cardinal symptoms
Oseltamivir if evidence influenza
NPPV if ventilatory failure
intubation if NPPV failed or contraindicated
COPD exacerbation. MCC?
upper respiratory infection
COPD exacerbation. moderate exacerbation, how defined?
Moderate exacerbation: 2 or more cardinal symptoms.
COPD exacerbation. JVP?
Jugular venous distention noted during expiration.
COPD exacerbation. Abs?
Antibiotics (3-7 days): azithromycin, respiratory fluoroquinolones, or penicillin/beta-lactamase inhibitors (amoxiclav).
COPD exacerbation. bronchodilators 2?
Bronchodilators: albuterol and ipratropium.
COPD exacerbation. steroids 2?
Steroids: PO prednisone or IV methylprednisolone.
▪ Given for 5 days.
▪ Improve lung function and hypoxemia, decreased risk of relapse, treatment failure, and length of hospital stay.
COPD exacerbation. altered mental status indicates what?
hypercapnia
COPD exacerbation. mild treatment combination?
Mild: MDI albuterol and ipratropium and PO prednisone.
COPD exacerbation. severe treatment combination?
Severe: Nebulizer albuterol and ipratropium IV methylprednisolone.
COPD exacerbation. severe treatment –> gets better?
▪ Gets better –> home. PO CS and MDI.
COPD exacerbation. severe treatment –> gets worse?
Gets worse (rising CO2, absent lung sounds) –> ICU.
IV CS, and nebulizer.
Preferred method of respiratory support is NPPV. If fails –> invasive mechanical ventilation.
o Required in hypercapnic patients with poor mental
status, hemodynamic instability, or profound acidemia
(pH <7.1).
COPD exacerbation. severe treatment –> needs more time to evaluate?
Needs more time –> ward.
PO CS and nebulizer.
PFT. table. normal FEV1?
> 80 proc. (of predicted)
PFT. table. normal FVC?
> 80 proc. (of predicted)
PFT. table. normal FEV1/FVC?
> 70 proc
PFT. table. OLD FEV1?
decreased
PFT. table. OLD FVC?
normal to decreased
PFT. table. OLD FEV1/FVC?
decreased
PFT. table. restrictive (including obesity) FVC?
decreased
PFT. table. restrictive (including obesity) FEV1?
decreased
PFT. table. restrictive (including obesity) FEV1/FVC?
normal to increased
Therapeutically relevant to differentiate between COPD and asthma since inhaled steroids are the primary long-term intervention for asthma and a long-acting anticholinergic inhaler is preferred for COPD.
.
COPD exacerbation. ABs duration?
3-7 days
COPD exacerbation. 3 abs groups?
Macrolides (eg azithromycin)
Resp fluoroquinolones (levoflox, moxiflox)
Penicillin/beta-lactamase inhibitors (amoxiclav)
COPD exacerbation. symptomatic hypercapnia. what symptom cause initial suspicion? what to do?
Altered mental status in the setting of COPD exacerbation should raise suspicion for symptomatic hypercapnia
DO ABG
COPD exacerbation. symptomatic hypercapnia. pathophysiology?
a. Some patients with COPD retain CO2 during an exacerbation due to shallow breathing and high levels of ventilation-perfusion mismatch
b. Hence, despite tachypnea, patient may be hypercapnic
COPD exacerbation. symptomatic hypercapnia.
Symptomatic hypercapnia may present without significant hypoxemia.
.
COPD exacerbation. symptomatic hypercapnia. mild to moderate hypercapnia symptoms?
headache
hypersomnolence
COPD exacerbation. symptomatic hypercapnia. severe hypercapnia symptoms? (eg > 75-80 mmHg)
i. Delirium
ii. Confusion
iii. Lethargy
iv. Coma (CO2 narcosis)
v. Seizures
OXYGEN-INDUCED CO2 RETENTION IN COPD. schema jau buvo anksciau. what changes in brain hormones when acidosis?
- Acidosis caused by an acute increase in CO2 leads to altered level of consciousness due to following changes in the brain:
a. incr. GABA and glutamine
b. decr. Glutamate and aspartate
OXYGEN-INDUCED CO2 RETENTION IN COPD. what hormones in brain incr in case of acidosis?
GABA and glutamine
OXYGEN-INDUCED CO2 RETENTION IN COPD. what hormones in brain decr in case of acidosis?
glutamate and aspartate
OXYGEN-INDUCED CO2 RETENTION IN COPD.
Hypercapnia -> Cerebral vasodilation
-> Seizures
.
OXYGEN-INDUCED CO2 RETENTION IN COPD.
prevention of CO2 retention?
a. Oxygen should be cautiously used with following goals:
i. SaO2 of 90%-93% OR
ii. PaO2 60-70 mm Hg
b. Patients who develop significant acidosis or have severely reduced level of consciousness require mechanical ventilation
