Study and complete the following Mini Clini: Differentiating Causes of Hypoxemia. Explain the pathophysiological mechanism of how the following disorders cause hypoxia:

• Pleural effusion
• Parkinson's Disease
• Guillian Barre

Write a 400-500 word summary and use at least one scientific/medical resource for support.

Use standard essay format in APA style, including an introduction, conclusion, and title page. Cite in-text and in the References section.

Mini Clini: Differentiating Causes of Hypoxemia

Problem:

Two patients present with the following ABGs at sea level:

Patient A

pH                   7.45

PaCO₂ 33mmHg

PaO₂                40mmHg

HCO₃              22mEq/L

SaO₂                70%

FIO₂                0.21

Patient B

pH                   7.21

PaCO₂             72mmHg

PaO₂                53mmHg

HCO₃              28mEq/L

SaO₂                81%

FIO₂                0.21

1. Define the respiratory condition indicated by each ABG analysis.

2. What is the P(A-a)O₂ for each blood gas?

3. Identify the type of respiratory failure in each of those cases.

4. In which case would administration of 100% FIO₂ help determine therapy?

Discussion:

1. Patient A exhibits uncompensated respiratory alkalosis with hypoxemia. Patient B exhibits partially compensated respiratory acidosis with hypoxemia.

2. Patient A:

PaO₂=0.21(760-47)-33/0.8=108mmHg

PaO₂=40mmHg

P(A-a)O₂=108-40=68mmHg on room air

Patient B:

PaO₂=0.21(760-47)-72/0.8=60mmHg

PaO₂=53mmHg

P(A-a)O₂=60-53=7mmHg on room air

The normal values for P(A-a)O₂ range from 10mmHg in young people to approximately 25mmHg in the elderly while breathing room air.

3. Patient A is a case of hypoxemic respiratory failure (type I) as characterized by the below normal PaO₂ (40mmHg). The PaCo₂ is also below normal (33mmHg) indicating hyperventilation is taking place in an effort to improve the oxygenation. Patient B is a case of hypercapnic respiratory failure (type II) as characterized by the above normal PaCO₂ (72mmHg) indicating hypoventilation (ventilatory failure) is occurring. This is also known as acute ventilatory failure superimposed on chronic ventilatory failure. This patient is also hypoxemic (53 mmHg). There is a slight elevation of the HCO₃ (28mEq/L) indication an element of chronic respiratory failure may be present, which has now become acute.

4.Patient A has hypoxemic respiratory failure with a P(A-a)O₂ of 68mmHg, which is well above normal, indicating an oxygenation defect. The administration of 100% O₂ in this case would help to determine the cause of the defect. Significant response to the 100% FIO₂ would point to V/Q mismatch as the cause, while shunt would be implicated if the PaO₂ did not respond to the increase in delivered O₂. In the latter, some form of PEEP would be necessary to improve gas exchange by improving FRC.

Patient B has hypercapnic respiratory failure (ventilatory failure) with hypoxemia, but with a P(A-a)O₂ of 7mmHg which is within the normal range. This indicates a pure ventilatory defect as the cause of the hypoxemia, and administration of 100% FIO₂ would not help to determine therapy. Depending on the full patient scenario, this patient may require intubation and mechanical ventilation to restore normal acid-base status.