60. Chronic obstructive pulmonary disease Flashcards
COPD defn
common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.
Most important copd rf?
smoking
COPD RF
smoking
>40
male
occupational exposure
indoor air polution
genetics like alpha 1 antitrypsin
copd: what determines severity?
spirometry
Bronchioles terminate in a functional lung unit called ?__
acinus
Acinus is supplied by a respiratory bronchiole and includes what 2 alveolar things?
sac
ducts
In COPD, what causes airflow R?
progressive changes to bronchial tree and lung parenchymia by inflamm which leads to remodeling, destruction via oxidative stress and protease
also incr mucous production, submucosal gland enlargement, goblet metaplasia, decreased mucociliary clearance
Neutrophil elastase - how does this play a role in COPD?
enzyme destroys neutrophils that normally make matrix of lung parenchyma (upregulated from inflammation in disease)
alpha 1 antitrypsin actually stop s enzyme from working, but in copd this can also become deficient
What is emphysema?
pathological dx - destruction of lung parenchyma
What symptoms/signs does emphysema cause? (2 broadly)
gas trap
airflow obstruction
Difference in emphysema location alpha 1 antitrypsin copd vs smoking copd
Patients with alpha 1-antitrypsin deficiency usually have panacinar emphysema predominantly in the lower lung zones,
whereas chronic smokers typically have central aci- nar emphysema predominantly in the upper lung zones
Chronic bronchitis defn
cough and sputum production most days over 3 months for at least 2 years
What does chronic bronchitis occur in copd?
incr mucous production
decreased ciliary clearance
chronic bronchial inflamm
Why do patients with COPD potentially get pulmonary hypertension?
Chronic hypoxia secondary to lung parent time of destruction laid in the course of COPD. This leads to vas a construction of the small vessels of the pulmonary arterial bed, and resulting in vascular remodeling, hyperplasia, smooth muscle, hyperplasia, and hypertrophy.
As such, this may lead to cor pulmonale and right ventricular remodelling
What are the results of COPD patients in terms of residual volume, functional residual capacity, total lung capacity
Increased
Meaning of there is more dead space and a decline enforced expiratory volume in one second because of the loss of lung tissue and loss of elastic recoil.
What symptoms my patients have COPD present with?
Progressive dyspnea.
Chronic cough or speed of production.
Recurrent lower respiratory tract and infection
Gold one severity, classification airflow, limitation, and patients with COPD: FEV one?
Mild
FEV one greater than equal to 80% predicted
Gold two severity, classification airflow, limitation, and patients with COPD: FEV one?
Moderate.
Between 50 to 80% of predicted FEV one
Gold three severity, classification airflow, limitation, and patients with COPD: FEV one?
Severe
Between 30 to 50% of FEV1 predicted
Gold four severity, classification airflow, limitation, and patients with COPD: FEV one?
Very severe
Less than 30% of EUV one predicted
Gold classification of COPD, incorporates, the severity of which thing? (4)
Severity of spirometry abnormalities.
Nature and magnitude of symptoms.
History of moderate exacerbation.
Comorbid conditions
If a patient has a moderate to severe exacerbation, history ( Greater than equal to two exacerbations, greater than or equal to one leading to hospitalization) and mild symptom burden, what classification are they?
C
If a patient has a moderate to severe exacerbation, history ( Greater than equal to two exacerbations, greater than or equal to one leading to hospitalization) and severe symptom burden, what classification are they?
D
If a patient has a mild exacerbation, history ( none or one Not leading to hospitalization) and mild symptom burden, what classification are they?
A
If a patient has a mild exacerbation, history ( none or one Not leading to hospitalization) and severe symptom burden, what classification are they?
B
What is the most common bacterial infection in COPD?
H influenza
Streptococcus, pneumonia.
Moraxella
Classification of respiratory failure, and COPD exacerbation: signs of no respiratory failure
Mild tachypnea with a rate of 20 to 30 breast per minute.
Normal with the breathing.
Baseline mental status.
Mild hypoxia response to oxygen by nasal cannula.
No hypercarbia
Classification of respiratory failure, and COPD exacerbation: signs of acute respiratory failure
Significant respiratory rate with rate of greater than 30 breath per minute
Increased work and breathing with accessory muscle use
Baseline mental status.
Hypoxemia responsive to supplementation with less than 35% FiO2.
Hypercapnia with PACO2 50 to 60 and PH greater than 7.25
Classification of respiratory failure, and COPD exacerbation: signs of severe respiratory failure
Altered mental status.
Hypoxemia requiring supplementation with greater than 35% FiO2
PA CO2 greater than 60 or pH less than 7.25
Why do patients with COPD get respiratory failure?
Often change to purse slip, breathing in order to try to increase the gradient from alveolar pressure to ambient air pressure, but in fact, this decreases exhalation time increasing the proportion of dead space ventilation, and has a high energy cost
This can cause dynamic hyper inflation, which occurs because there’s not enough expiratory time, leading to Alviola over distinction, increased inter, thoracic pressure and decreased lung compliance
Differential diagnosis of an acute chronic obstructive, pulmonary disease exacerbation
Infection: pneumonia, plural, effusion, pulmonary oedema
Other lung: pneumothorax, pulmonary embolism, metabolic acidosis with compensatory resp rate
Cardiac : cardiac arrhythmia, pericardial, effusion, heart failure
Neoplasm – malignancy
Lab tests and investigations for chronic obstructive, pulmonary disease and it’s differential
Chest x-ray and if concern for PE or otherwise CT
Pulse ox
Blood gas
ECG
CRP
What ECG findings or rhythms are common in a COPD exacerbation
Tachycardia.
A fib.
Atrial flutter.
Multifocal atrial tachycardia.
Ventricular arrhythmias- higher risk than general public
Signs of P pulmonale for patients with COPD on ECG
Large greater than 2.5 mm peaks tea waves in leads two, three and AVF and greater than 1.5 mm in V1 and two, low QRS voltage and poor wave progression of less than 3 mm in V3
What medication should you give in a COPD exacerbation?
Short acting, beta agonist
Short acting anticholinergic
Five day course of prednisone if able to do PO or methyl prednisolone, if not
Antibiotics if you are concerned for a specific bacterial infection: amoxycillin clave seven day course, macrolide five day course, tetracycline seven day course
What adjective treatments are important in COPD exacerbation
Smoking cessation
Inhaler technique.
Up-to-date, influenza and pneumococcal.
Vitamin D, check and supplement.
What should supplemental oxygen be titrated to in terms of PA O2 and oxygen saturation for a COPD exacerbation?
PAO2 of greater than 60
Peripheral oxygen saturation between 88 and 92%
Why in COPD exacerbation do patients need an oxygen saturation between 88 and 92%?
Changing the ventilation and perfusion ratios by altering hypoxic vasoconstriction to under ventilated lung zones
Some patients may require a hypoxic respiratory drive, but not all
Some contribution to hypercapnia may include the Haldane effect: high oxygen tension induces a right shift in the CO2 dissociation curve, therefore increasing the PAC 02
What is first line therapy for a patient with an acute COPD exacerbation with respiratory failure?
High-level non-invasive ventilation
Indications for bilevel non-invasive ventilation: three
One. Respiratory acidosis with a PACO2 greater than equal to 45 and a pH less than or equal to 7.35.
Two. Severe shortness of breath with signs of respiratory muscle, fatigue, and accessory muscle use.
Three. Persistent hypoxia, despite supplemental oxygen therapy.
Indications for switching to a invasive, mechanical ventilation in a COPD exacerbation
- Unable to tolerate non-invasive ventilation
Non-invasive ventilation failure.
Persistent diminished consciousness.
Respiratory or cardiac arrest.
Persistent, inability to remove remove secretions.
Hemodynamic instability without response to fluids and Vaso active medication.
Life-threatening hypoxia not corrected by less and invasive interventions.
Contraindications: bilevel noninvasive ventilation
Active emesis or high risk aspiration.
Respiratory arrest
Facial trauma.
Depressed mental status, not related to a high PA CO two
Invasive, mechanical, ventilation contraindications
Appropriate for noninvasive ventilation
Patient wishes
Why is non-invasive ventilation helpful in a COPD exacerbation?
Offload respiratory muscles to help aid in the work necessary to overcome the intrinsic positive and expiratory pressure
Decreases the respiratory rate to allow more effective emptying of the lungs and a patient can take breaths with larger title volumes to improve alveolar ventilation
Settings for high-level positive pressure, ventilation:
Inspiratory positive airway pressure 12 to 15 cm of water.
Expiratory positive airway pressure of 5 cm through a facemask.
Inspired auction should be titrated between 88 to 92%
Inspiratory to expiratory ratio of one to four
Title volume around 6 to 8 mL per kilogram per minute
For an intubated patient, what should you set the ventilator mode to and settings: for a COPD exacerbation
Assist control motive ventilation
Respiratory rate 10 to 14 breast per minute
Title volume of less than equal to 8 mL per kilogram of predicted body weight.
Inspiratory time of 0.8 to 1 seconds.
Positive and expiratory pressure of five
Titration inspired oxygen to saturation of 88 to 92%
If a patient with a COPD exacerbation who is intubated has an elevated peak pressure greater than 40 to 45 cm of water white reversible causes should I look for? 3
Mucus plug.
Kinked or malpositioned endotracheal tube.
Tension, pneumothorax
What is my goal plateau pressure for a COPD exacerbation intubated patient
Less than 30
What is dynamic hyper inflation?
Occurs when the patient receives a breath before the respiratory system returns to FRC i.e. complete exhalation and increases and expiratory, lung volumes and interest thoracic pressure
What are signs of dynamic hyper inflation?
Flow versus thyme wave form – if expiratory flow limb does not reach zero prior to the next breath there will be dynamic hyper inflation
And expiratory velocity.
Total peep: measured after a 3 to 52 and expiratory hold on a passively breathing patient – patient seer intubated during a COPD exacerbation without multiple pulmonary infiltrates should have a normal plateau pressure despite an increase in peak pressure
COPD exacerbation: pressure assist control option for ventilation: pressure above peep, inspiratory cycling time, titled volume are recommended?
Pressure of 15 cm of water above peep.
Inspiratory cycling time of 0.8-1 second
8 mL per kilogram predicted bodyweight
The spontaneously breathing patient may be transition to pressure support, ventilation, and COPD exacerbation: recommended initial pressure support above peep?
Peep setting overall
15 cm of water above peep titrated based on title volume and patient comfort.
Peep can be safely set to 5 cm of water
Troubleshooting ventilation difficulties in intubated patients with chronic obstructive, pulmonary disease:
Elevated end title CO2 or PA CO2
Tolerate respiratory acidosis of the pH is greater than 7.2 without adjusting the respiratory rate or title volume.
Respiratory acidosis will improve with medical treatment and time while ventilated
Troubleshooting ventilation difficulties in intubated patients with chronic obstructive, pulmonary disease:
Elevated entitle CO2 or Pa CO2 and pH of less than 7.2
If there is minimal intrinsic, PEEP, increase the respiratory rate slowly and frequency check for intrinsic PEEP
Should intrinsic peep develop, increase the title volume and keep the rate low. The goal is less than equal to 8 mL per kilogram of predicted bodyweight, if severe respiratory acidosis and obstructive shock from dynamic hyper inflation is a threat to Leif, start increasing title volume.
Troubleshooting ventilation difficulties in intubated patients with chronic obstructive, pulmonary disease:
High peak pressures
This is a reflection of increased airway resistance. Check a plateau pressure to evaluate compliance of the respiratory system. If the plateau pressure is low:
Evaluate for a common cause of elevated peak pressure, including kinked tubing, new pneumothorax, mucus, plugging, main stem, intubation, continue bronchodilator therapy and tolerate high peak pressures. Increase peak pressure alarm to prevent hypo ventilation.
If the patient does not have a reason to have low compliance, then this is likely representing Alviola over distinction from dynamic hyper inflation. Check a total peep and decrease the minute ventilation.
Troubleshooting ventilation difficulties in intubated patients with chronic obstructive, pulmonary disease:
Elevated total peep, or intrinsic peep:
This represents dynamic hyper inflation.
If hypertension is present, remove the patient from the ventilator for approximately 10 to 15 seconds to allow for adequate acceleration.
Reduce the minute ventilation by decreasing the respiratory rate between 10 and 14 breaths per minute
Troubleshooting ventilation difficulties in intubated patients with chronic obstructive, pulmonary disease:
Awakens from sedation or paralysis wears off
Clinical decision of transition to a pressure, supported motive, breathing or increasing sedation.
If stable, patient will often tolerate pressure support ventilation within initial setting a pressure support of 15 cm of water over a peep of 5 cm of water. Patient will determine their respiratory rate. Monitor for triggering or cycling synchronies such as the patient trying to inhale or exhale and the ventilator not responding.
If the patient is unstable or has severe air trapping, sedation of the patient is synchronous with the ventilator. Re-attempted sedation wean at a later time.
If any changes to peep are made, what three things do do I also need to check?
Peak pressure.
Total peep.
Plateau pressure
When should admission be considered for a patient with chronic obstructive pulmonary disease? Five.
One. Significant worsening of symptoms from baseline.
Two in adequate response of symptoms to emergency department management
Three significant comorbid conditions.
Four worsening hypoxia hypercarbia from baseline.
Five in ability to cope Home or insufficient resources.
A patient presents to the emergency department with eight months of progressive shortness of breath. There is no recent change in the patient symptoms. On exam there’s a prolonged expiratory phase without wheezing, no rails, no pedal edema. The electrocardiogram is normal and the chest x-ray reveals hyper inflation with a flat and diaphragm. The diagnosis of COPD:
A can be made clinically in this patient.
B can be made radiographically.
C requires demonstration of spirometry.
D requires genetic testing
C
In a patient with a diagnosis of COPD, decreased dyspnea, sputum, production, and speed of parlance worse than baseline day-to-day variation for the past three days requiring a evaluation in the emergency department is defined as
COPD exacerbation
A 64-year-old male presents to the emergency department with a history of severe, chronic obstructive, pulmonary disease and a baseline of 3 L pitted oxygen requirement with a complaint of dyspnoea on exam he has a respiratory rate of 50, requiring 8 L per minute by nasal canula to maintain an SPO2 of 88% but awaken following commands, a blood gas shows a pH of 7.25 and a PCO2 of 70. Chest x-ray reveals hyper inflation without any other cause. Antibiotics, nebulized short, acting, beta, agonist and glucocorticoids are initiated. The next step in management is
Continue medical management.
B intubate the patient anticipated clinical decline
C start not in bases by level positive pressure ventilation
D trial high flow, nasal canula
C
The Rachella breathing pattern that develops in a chronic obstructive, pulmonary disease exacerbation? Inhalation time, causing hyper inflation and? The proportion of dead space, ventilation, causing hypercapnia and respiratory muscle.
Decreases
Increases
When trading a patient with COPD exacerbation who requires invasive, mechanical ventilation, setting the initial title volume of 8 mL per kilogram predicted bodyweight, and a respiratory rate of 10 to 14 breast per minute, helps prevent the development of.
A acidosis.
B dynamic hyper inflation
C hypercapnia
D expiratory flow limitation
B
