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8. What are the typical clinical manifestations/ patient assessment data? (relate these to pathophysiology concepts already described)

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8. What are the typical clinical manifestations/ patient assessment data? (relate these to pathophysiology concepts already described)

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Inspection
Hyperinflation - Barrel Chest from air trapping (Increased Anterior-Posterior diameter), Flattened diaphragm
Use of accessory respiratory muscles - due to respiratory distress
Hoover's Sign - Inspiratory retraction of the lower intercostal spaces that occurs with obstructive airway disease
Pursed lips - Effort to slow down the expiratory phase and this is needed to help get air out of the lungs.

Auscultation
Reduction of lung sounds - Due to airflow limitation and poor transmission of sounds due to the destruction of parenchyma
Expiratory Wheezing - Prolonged expiration (increases pressure in the airways; keeps airways from collapsing)

Hypoxic vasoconstriction due to poor gas exchange in the alveoli can lead to pulmonary hypertension (more work for the ride side of the heart) in turn leading to enlarged/right sided heart failure.
Signs of RHF
- Elevated jugular venous pressure
- Peripheral oedema can be observed

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1. Choose a spokesperson

2. All students in the group are to work on all of the following questions/sections included in the Padlet

3. You can use diagrams/images other visual resources to explain each respiratory condition.

4. When we come back to the whole class, the spokesperson will feedback the groups findings, with the teams support

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Pulmonary emphysema, a progressive lung disease, is a form of chronic obstructive pulmonary disease (COPD). It is a disorder affecting the alveoli of the lungs. In emphysema, the alveoli become abnormally inflated, damaging their walls and making it harder to breathe. Symptoms include shortness of breath, coughing and fatigue.

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4. Explain the role of V/Q mismatch in this condition.

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4. Explain the role of V/Q mismatch in this condition.

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Gas exchange is reduced in COPD by:

Emphysema reduced the elasticity of alveoli and as such can lead to air trapping and reduced surface area for diffusion or dead space. This results in low ventilation and normal perfusion (V/Q mismatch).

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5. How is oxygenation and ventilation affected? Eg. consider O2 content, O2 delivery, alveolar ventilation 

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5. How is oxygenation and ventilation affected? Eg. consider O2 content, O2 delivery, alveolar ventilation 

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(V/Q) mismatch results from progressive airflow limitation and  destruction of the pulmonary capillary bed.

Oxygen delivery: Delivering too much oxygen to patients with (COPD) with hypercapnia can cause hyper oxygenation and can reduce their hypoxic respiratory drive and n turn cause respiratory failure.

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2. Is it obstructive or restrictive? Why?

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2. Is it obstructive or restrictive? Why?

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It is Obstructive
Small airways collapse when you exhale, impairing airflow out of your lungs. At the end of a full exhalation, an abnormally high amount of air may still be present in the lungs.

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3. How does the condition effect lung compliance and/or airway resistance?

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3. How does the condition effect lung compliance and/or airway resistance?

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In COPD there is higher compliance of the lungs due to damage of elastic recoil of the alveoli and surrounding tissue. This can be caused by genetic factors (alfa-1 antitrypsin deficiency) or external factors (smoking).

Airway resistance is the change in pressure needed to produce air flow into the lungs. It is essentially a physiological airway obstruction. In COPD the damaged walls of the alveoli can make it more difficult to facilitate airflow, in turn reducing the patients ability to create enough pressure to fill the alveoli (take a breath).

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6. What type of respiratory failure would this condition lead to?

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6. What type of respiratory failure would this condition lead to?

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Can lead to both T1 (initially) and T2 (over time) with extreme hypoxia and hypercapnia
- there is a matched VQ deficit ie. both ventilation and perfusion are decreased therefore gas is impaired going in (O2) and coming out (CO2)
- air can become trapped in alveoli after expiration
- breakdown of alveoli leads to decr surface area for diffusion to occur

Hypoxaemia (T1RF) can result from decreased diffusion and gas exchange at the alveoli. This occurs due to the destruction of aveolar wall and capillary bed resulting in decr surface area for adequate gas exchange to occur

Hypercapnic T2RF can occur for a similar reason- the decreased surface area due to alveolar destruction means that more CO2 is retained in blood instead of diffusing out. However, as CO2 is so readily diffused, hypercapnia can be a sign of more moderate-severe emphysema
There is also an obstructive component where air is impaired during exhalation, resulting in increased end expiratory volume and air retained in lungs instead of being exhaled

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pH- normal, compensatory mechanisms should ensure that the pH remains within normal limits. depending on the degree of hypercapnia and compensation, there may be an acidosis if compensation is no longer adequate or in an acute exacerbation.
pCO2- high/normal, in mild-moderate cases, CO2 may continue to diffuse out and therefore be normal, however as the diseases progresses and gas exchange and elastic recoil is severely limited, CO2 will rise causing hypercapnia
PaO2- low (70s) - due to decr gas exchange surface area and increased distance for oxygen to diffuse across
HCO3- - may be high as a chronic compensatory mechanism for hypercapnia

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9. OPTIONAL: Important vocabulary (include list of key vocabulary referenced; if you do not know the term(s), look up and add a definition for the word(s))

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9. OPTIONAL: Important vocabulary (include list of key vocabulary referenced; if you do not know the term(s), look up and add a definition for the word(s))