Mild hypoxemia with a fully compensated respiratory acidosis

92% – 100%The following 5 ABG analyses were formulated using Pierce’s (2007) systematic analyses (p.55 – 60). Normal values according to Pierce are listed as follows:

The systematic analysis is done by first looking at each number individually and labeling it. Second describing the adequacy of oxygenation by assessing PaO2 and SaO2. Pierce (2007) lists hypoxemia as mild (<80 mm Hg), moderate (<70 mm Hg) and severe (<60 mm Hg) and a SaO2 of below 92% as hypoxemia. Pierce (2007) then tells us in step 3 to determine the acid base status by assessing the pH. The fourth step involves deciding whether the acid base disorder is respiratory or metabolic and the final step is to determine the extent of compensation (p.57).

ABG #1

FiO2

0.21

pH

7.40

Normal

PaCO2

50

Acidemia

PaO2

71

Hypoxemia

HCO3

30.9

Alkalemia

BE

5.0

Alkalemia

SaO2

95.1

Normal

Hb

12.9

Mr. Puffin’s PaO2 of 71 shows mild hypoxemia, with a SaO2 within normal limits. His pH of 7.40 is neutral and shows that his acid base status is within normal limits; however his PaCO2 of 50 demonstrates that he is acidotic and his elevated HCO3 indicates compensation is occurring. These results suggest Mr. Puffin has a mild hypoxemia with a fully compensated respiratory acidosis. His normal pH indicates full compensation is occurring,

ABG#2

FiO2

0.50

pH

7.14

Acidemia

PaCO2

127

Acidemia

PaO2

44.2

Hypoxemia

HCO3

41.6

Alkalemia

BE

7.1

Alkalemia

SaO2

69.2

Hypoxemia

Hb

14.1

Mr. Puffin’s PaO2 and SaO2 show he has a severe hypoxemia. His pH of 7.14 is indicative that he is acidotic. His PaCO2 is elevated which shows the acidemia is respiratory in origin. The elevated HCO3 of 41.6 shows that metabolic compensation is occurring, therefore these results indicate Mr. Puffin has severe hypoxemia with a partially compensated respiratory acidosis.

ABG #3

FiO2

0.40

pH

7.22

Acidemia

PaCO2

99.6

Acidemia

PaO2

45.3

Hypoxemia

HCO3

39.9

Alkalemia

BE

8.3

Alkalemia

SaO2

Hb

ABG #3 shows Mr. Puffin’s respiratory acidosis has improved due to BiPAP therapy. There is a slight increase in his PaO2 although it still shows severe hypoxemia. His pH has improved but still shows acidemia. PaCO2 has decreased due to BiPAP therapy but remains elevated and indicates respiratory remains his primary cause of acidosis. Mr. Puffin’s HCO3 is also still elevated indicative of partial compensation occurring. ABG #3 shows Mr. Puffin still remains severely hypoxic, with a partially compensated respiratory acidosis.

ABG #4

FiO2

0.40

pH

7.32

Acidemia

PaCO2

71.9

Acidemia

PaO2

55.6

Hypoxemia

HCO3

36.1

Alkalemia

BE

8.0

Alkalemia

SaO2

Hb

ABG #4 shows further improvement in Mr. Puffin’s severe hypoxemia and respiratory acidosis. His PaO2 has increased further but still shows a severe hypoxemia. His pH although increased still suggests mild acidosis, as well as his PaCO2 of 71.9, although it has decreased, still indicates a respiratory origin. HCO3 remains elevated showing compensation is occurring; therefore Mr. Puffin still has severe hypoxemia with a partially compensated respiratory acidosis.

ABG #5

FiO2

0.28

pH

7.00

Acidemia

PaCO2

59.1

Acidemia

PaO2

62.4

Hypoxemia

HCO3

18

Acidemia

BE

-7.8

Acidemia

SaO2

92%

Hb

14.2

Mr. Puffin’s 5th ABG PaO2, indicates moderate hypoxemia. His pH is low and shows he is acidotic. An elevated PaCO2 suggests acidemia respiratory in nature. HCO3 is also low which also shows acidemia metabolic in nature. Mr. Puffin in ABG #5 has a moderate hypoxemia with a mixed respiratory and metabolic acidosis confirmed by the decreased BE.

Question Two:

What type of respiratory failure does Mr. Puffin have?

Provide a rationale for your answer based on the clinical information supplied.

Differentiate between Type 1 and Type 2 Respiratory failure.

Respiratory failure as described by Pierce (2007) is the “absence of the normal homeostatic state of ventilation as it relates to acid – base status of the blood and the exchange of oxygen and carbon dioxide” (p.181).

Type 1 respiratory failure, Pierce (2007), describes as a “failure to oxygenate or hypoxemic respiratory failure, categorized by a PaO2 of less than 60mm Hg on an FiO2 of more than 0.5”, and Type 2 respiratory failure as “failure to ventilate, also called ventilatory failure, hypercapnic respiratory failure, or respiratory pump failure, as a PaCO2 of greater than 50mm Hg, with a pH of 7.25 or less” (p.181-182).

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In contrast to Pierce’s definition Hennessey & Japp (2007) define respiratory failure as respiratory impairment. Hennessy & Japp define type 1 respiratory impairment as low PaO2 with normal or low PaCO2 which implies defective oxygenation despite adequate ventilation and the PaCO2 is low due to compensatory hyperventilation (p.20). Hennessey & Japp (2007), define type 2 respiratory impairment as a high PaCO2 (hypercapnia), and is due to inadequate alveolar ventilation, and since oxygenation also depends on ventilation, the PaO2 is usually low, but may be normal if the patient is on supplemental oxygen (p.22).

Type 1 respiratory failure is most commonly caused by VQ mismatch, pneumonia, pulmonary embolism, pneumothorax, pulmonary edema, shunt and acute respiratory distress syndrome and initial treatment is aimed at achieving an adequate PaO2 and SaO2 with supplemental O2 while attempting to correct the underlying cause, Hennessey & Japp (2007) p. 20.

Type 2 respiratory failure is commonly caused by chronic obstructive pulmonary disease, exhaustion, flail chest injury, opiate/benzodiazepine toxicity, neuromuscular disorders and obstructive sleep apnea, with clinical signs that include confusion, drowsiness.

Based on the case study information it is evident Mr. Puffin has Type 2 respiratory failure. The diagnosis of type 2 respiratory failure could be made through the interpretation of ABG #2 as he has a decreased pH and elevated PaCO2 with hypoxemia. His presentation of his difficulty breathing, productive green cough, drowsiness and confusion are consistent with the presentation of an acute exacerbation of chronic obstructive pulmonary disease due to his previous diagnosis made by his doctor of emphysema.

Question Three:

What is BiPAP?

BiPAP (Bi – Level Positive Airway Pressure) is a form of non – invasive mechanical ventilation commonly administered to patients with exacerbations of type 2 respiratory failure, that delivers two airway pressures through inspiration, (IPAP), and expiration, (EPAP) measured in cm H20. IPAP is the abbreviation for Inspiratory Positive Airway Pressure and EPAP is the abbreviation for Expiratory Positive Airway Pressure.

BiPAP is delivered to the patient through an appropriate bilevel ventilator eg Vision BiPAP, or Respironics BiPAP, through a nasal mask, full face mask, or total face mask.

Describe the effects of BiPAP.

In your answer consider its effects on airway pressures, the alveoli, the lung,

and the cardiovascular and neurological systems.

When BiPAP is administered to a patient with type 2 respiratory failure, during inspiration (IPAP) a higher level of positive airway pressure is delivered, increasing breath size, which helps to clear out carbon dioxide and assumes a fatigued patients work of breathing, and during expiration (EPAP) prevents atelectasis, recruits collapsed alveoli and enables gas exchange between breaths (Woodrow 2003). The difference between IPAP and EPAP is termed pressure support so for example if Mr. Puffin was commenced on 12 cm H20 IPAP and 6 cm H20 EPAP he would have 6 cm H20 being the being the difference between 12 and 6 of pressure support. Pressure support decreases the work of breathing by initiating breathing and increasing tidal volume.

Question Four:

Outline the clinical indications for the use of BiPAP in Mr Puffin’s case.

Discuss the monitoring that would be required for the safe application of

BiPAP.

List the possible complications of BiPAP that may occur in Mr Puffin’s case.