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Cardiogenic acute pulmonary oedema is fluid accumulation in the lungs which impairs gas exchange and lung compliance. Left ventricular failure will cause increase capillary hydrostatic pressure within pulmonary circulation due to back flow. Drawing fluid out of the intravascular space into the interstitial space and the alveoli.

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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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Restrictive as fluid prevents alveoli inflating sufficiently. Fluid also causes decreased compliance of lung tissue. It decreases the total volume of air the alveoli can hold.

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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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Decreases compliance as the alveoli have a harder time expanding and higher chance of collapsing due to high surface tension in the alveoli.

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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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In cardiogenic acute pulmonary oedema, adequate perfusion to alveoli but impaired ventilation due to fluid would show a low VQ ratio (less than 0.8).

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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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Oxygenation is impaired as oxygen has trouble diffusing from the alveoli to capillaries due to the build up of fluid, causing low SpO2. Alveolar oxygen content (AO2) may be high, however it is unable to move into the capillary space, causing low aO2 (high Aa gradient). Ventilation may be adequate.

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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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- dyspnea, worse on exertion & lying down, needing to work harder to adequately ventilate
- Use of accessory muscles
- Diaphoretic
- Anxious, restless
- Increased RR, compensating to increase oxygen levels
- Decreased SpO2, due to ineffective gas exchange
- Decreased tidal volume, the alveoli has less capacity for air
- Can cause V/Q mismatch, the is inadequate ventilation
- Crackles on auscultation, movement of air over fluid and bubbles
- ECHO - L) sided dysfunction
- CXR - areas of opacity - fluid
- Cyanosis
- Tachycardia
- Hypertension
- Peripheral oedema secondary to R)HF caused by APO

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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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Initially T1RF due to hypoxia with normal CO2, however can lead to T2RF as the patient becomes fatigued and more unwell due to less expiration of CO2 (hypoxic & hypercapnic).

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- pH: initially alkalotic (high pH caused by low CO2 level due to tachypnoea), then acidotic (low pH) due to CO2 retention
- Low Pa02
- Initially low PCO2, then higher
- Bicarbonate: May be normal initially, as the patient becomes acidotic and over days, bicarbonate may increase to compensate