Week 8: Obstructive Pulmonary Disease

Question 1

What is Hypoxemia?

Answer 1

Typically caused by pulmonary disease, it results in there not being enough oxygen in the blood due to ventilation-perfusion abnormalities (i.e., shunting, alveolar dead space)

Question 2

What is Hypercapnia?

Answer 2

Typically caused by pulmonary disease, it results in the increase of carbon dioxide in the blood and occurs from a decreased drive to breather or an inadequate ability to respond to ventilatory stimulation.

Question 3

Explain the etiology, pathophysiology, manifestations, and complications of Asthma

Answer 3

Asthma is a common, chronic respiratory disease involving airway hyper responsiveness to direct or indirect stimuli, with chronic airway inflammation. characterized by variable symptoms of wheezing, shortness of breath, chest tightness, and/or cough, and by variable expiratory airflow limitation. Chronic inflammation of the bronchial mucosa causes bronchial hyper-responsiveness, constriction of the airways and variable airflow obstruction. Asthma involves smooth muscle constriction, making the lumen and bronchioles smaller, degranulation of mast cells, contributing to edema and mucus. If mucus plugs and obstructs a bronchiole, you might see hyper-inflation of the alveoli (air gets trapped).

Question 4

Explain the etiology, pathophysiology, manifestations, and complications of COPD

Answer 4

Chronic obstructive pulmonary disorder results from gene-environment interactions occurring over the lifetime of the individual that can damage the lungs and/or alter their normal development/aging process. It is a heterogeneous lung condition characterized by chronic respiratory symptoms (dyspnea, cough, sputum production and/or exacerbations) due to abnormalities of the airways (bronchitis, bronchiolitis) and/or alveoli (emphysema) that causes persistent, often progressive airflow obstruction. The best documented risk factor is a severe hereditary alpha-1 trypsin deficiency (AATD) which is the major circulating inhibitor of proteases; if you have COPD and AATD, your progression of the disease will be worse. In COPD you will see air trapping, where the alveoli become damaged (stretched out like an elastic) and will fill but can’t bounce back to push the air out of the lungs. There will also be pulmonary gas exchange abnormalities and pulmonary hypertension. Primarily, COPD is characterized by chronic bronchitis and emphysema. Clinical manifestations of COPD include dyspnea, barrel chest (hyperresonate sounds with percussion), use of accessory muscles to breathe, chronic cough, and pulmonary hypertension resulting in right ventricular enlargement and right-sided heart failure (cor pulmonale)

Question 5

Discuss important ABG measurements in chronic obstructive pulmonary disease

Answer 5

In COPD we will see a decrease in PO2 and an increase in PCO2 as the pH lowers and becomes more acidic, resulting in respiratory acidosis. HCO3- increase will be found in later stage COPD as the metabolic system attempts to compensate!

Question 6

What is pulmonary function and how is it measured

Answer 6

Testing pulmonary function includes:
1. Spirometry:
- FVC: forced vital capacity (have the patient breathe in and then breathe out) - normal is 5L
- FEV1: forced vital capacity in 1 second - normal is 4L
- FEV1/FVC Ratio: >0.75-0.80 in adults
2. Total lung capacity:
- sum of vital capacity and residual capacity
3. Thoracic imaging techniques
- chest radiography
- CT
- MRI
4. Arterial blood gas analysis
- determines pH and oxygen and CO2 concentrations

Question 7

Describe the function of the lung microbiome

Answer 7

There is accumulating evidence of cross-talk between the gut and the lungs; the upper GI microorganisms influence the airway microbiota primarily through aspiration. dysbiosis of the gut can lead to dysbiosis of the lung via microorganisms travelling through the blood stream.

Question 8

Describe the key differences between asthma and COPD

Answer 8

Asthma: is an obstructive pulmonary disease that has an early onset and is triggered by sensitizing agents (i.e., pet dander, dust), its symptoms vary from day to day. The inflammatory cells responsible for the symptoms of asthma are eosinophils and Cd4+ helper t-cells (allergen specific). Airflow limitation in this condition is usually reversible but may become persistent.

COPD: is an obstructive pulmonary disease that has a later onset and worsens progressively over time. It is triggered by noxious agents (typically smoking). The inflammatory cells responsible for the symptoms of COPD are neutrophils, macrophages and Cd8+ cytotoxic t-cells. Airflow limitation is not reversible.

Question 9

What is the V/Q ratio?

Answer 9

The ventilation/perfusion ratio is used to assess efficiency and adequacy of ventilation (the ability of air to reach alveoli) and perfusion (how well blood circulates and reaches alveoli via capillaries). Normally this ratio is 1:1 but a mismatch occurs when there is decreased ventilation but normal perfusions (i.e., asthma, lung injury, etc.) or when there is decreased perfusion but normal ventilation (i.e., pulmonary embolism)

Question 10

What are the 3 mechanisms of bronchoconstriction during an asthma attack

Answer 10

1. Sudden contraction of smooth muscle that causes acute dyspnea
2. Thick, viscous secretions
3. Edema - caused by engorgement of pulmonary blood vessels

Question 11

What is a late asthmatic response?

Answer 11

Begins 4-8 hours after the early response (the attack) and it involves the chemotactic recruitment of lymphocytes, eosinophils, basophils, neutrophils, and lymphocytes. This results in airway scarring, increased bronchial hyper-responsiveness, increased mucus function, decreased t-regulatory cells, and can lead to airway remodeling if left untreated.

Question 12

What is pulsus paradoxes?

Answer 12

when blood pressure drops significantly during inhalation and is related to changes in pressure in the chest; when pressure in the lungs and chest changes it can impact the pressure in and around the heart and blood pressure can drop. You might see a 10mm Hg drop on inspiration, this will impact the cardiovascular system.

Question 13

What is a silent chest?

Answer 13

no audible air-movement and a PCO2 greater than 70 mm Hg

Question 14

What happens with Alpha-1 antitrypsin deficiency?

Answer 14

AATD normally inhibits elastin after an inflammatory response, in the case of deficiency elastin will get uncontrollably released during inflammation, breaking down alveoli and creating damage.

Question 15

Why are patients with COPD more at risk for infections like pneumonia?

Answer 15

COPD patients are more at risk to get a respiratory tract infection due to mucus build up, creates a favorable environment for viruses and bacteria. The cilia are also damaged and unable to remove mucus and dead bacteria as well as product of inflammation. The body is therefore unequipped to adequately defend.

Question 16

Describe the difference between track 1 and track 2 asthma treatment for adults and adolescents

Answer 16

Track 1: uses inhaled cortico-steroids plus formoterol as the reliver reduces risks compared with using a short-acting beta-adrenergic reliver. This is the preferred approach and it is a simpler regimen for similar symptom control.

Track 2: uses an as needed short-acting beta-adrenergic reliver or an as needed inhaled cortico-steroid and a SABA. This is considered the alternative approach if track 1 is not possible or if a client’s asthma is stable with good adherence and no exacerbations in the past year on their current therapy. There are concerns with SABA only treatments increasing inflammation and allergic response and reduces bronchodilator response to SABA when it is needed.

Question 17

What treatment options are available for COPD?

Answer 17

Bronchodilators: use of long-acting formulations preferred, use of short-acting bronchodilators on a regular basis is not generally recommended in stable disease. However, as needed SABA use is beneficial in acute episodes. Combination therapy is considered gold standard. Bronchodilators alter smooth muscle tone and improve expiratory flow. They also reduce hyperinflation at rest, during exercise and improve performance - but they can’t change elastic recoil.

Inhaled Corticosteroids: regular treatment with ICS alone does not modify long-term decline of FEV1 or mortality. They may result in a higher prevalence of oral candidiasis, hoarse voice, skin bruising, and pneumonia. LABA and ICS combination is considered more effective and triple inhaled therapy of LABA/LAMA/ICS improves lung function symptoms and health status.