PFTs, ABGs, and RF in Obstructive and Restrictive Pulmonary Diseases

The major reason why I decided to write this essay was to show you how arterial blood gases and pulmonary function tests can help you in diagnosis and differential diagnosis of respiratory failure, obstructive and restrictive lung diseases.
This not a repetition of Drs Bellot and Jacobus’ lectures in Diseases of Respiratory System, this a comprehensive look on the problem, where I purposefully omitted some details; please excuse me if you find the omissions relevant or significant for the topic covered.
As you have learnt, the majority of pulmonary diseases, according to their major pathophysiologic mechanisms, can be divide two broad categories: obstructive and restrictive. I will start with definitions and major conceptual issues and then we proceed to lab findings.

Obstructive Lung Diseases
Obstructive diseases are characterized by reduction in ventilation due to increased airflow resistance as a result of
o Blockage of airways by mucus plugs (bronchial asthma and chronic bronchitis)
o Narrowing of airway lumina by hypertrophied and/or inflamed mucosa (chronic bronchitis)
o Bronchoconstriction (bronchial asthma)
o Loss of elastic recoil and impairment of expiratory flow (emphysema)
     -If you are interested in this mechanism look for a “equal pressure point” concept
Another component of respiration, perfusion, is less affected by obstructive lung diseases (except emphysema, which, by definition, is characterized by reduction in pulmonary vasculature).

How an increased resistance affects lung volumes?
1) Residual volume (RV) increases
     -RV – lung volume at the end of maximal exhalation
2) Vital capacity (VC) decreases
     -VC – volume that can be exhaled after a maximal inhalation
3) Total lung capacity (TLC) increases too because TLC = RV + VC, and an increase in RV is more that a decrease in VC
4) Forced vital capacity (FVC) moderately decreases because of increased airway resistance
     -FVC – volume that can be forcefully exhaled (during 5 sec) after a maximal inhalation. NB: understand the difference in TLC and FVC, which change in opposite directions
5) Forced expiratory volume in 1 sec (FEV1) significantly decreases because forceful expiration induced airflow turbulence with substantial reduction in flow rate
     -FEV1 – volume which is exhaled during the first second of FVC measurement
6) FEV1) / FVC ratio decreases [see explanation in 4) and 5)]

How an increased resistance affects ABGs?
Increased resistance to airflow leads to air retention in the lower airways with low PAO2 and high PACO2 (“A” – alveolar). Similar changes can be detected in the arterial blood: decreased PaO2 and increased PaCO2 (hypoxemia and hypercapnia).

How respiratory failure develops in patients with obstructive lung diseases?
At early stages of obstructive lung diseases, high concentration of carbon dioxide activates respiratory center that changes the pattern of breathing and maintains near- normal level of blood gases. With time and increased work of breathing, hypoxemia and hypercapnia rise and reach the levels of PaO2 < 60 mm Hg and PaCO2 > 50 mm, the condition is known as hypercapnic respiratory failure. High PaCO2 level lowers pH (respiratory acidosis) and activates bicarbonates retention by the renal tubules (metabolic compensation).

Restrictive Lung Diseases
This group is quite heterogeneous and is characterized by abnormalities in alveolocapillary interface, such as:
• Edema (pulmonary edema)
• Inflammation (pneumonia, ARDS, aspiration of gastric content)
• Fibrosis (idiopathic pulmonary fibrosis, pneumoconioses, sarcoidosis, etc)
Accumulation of pathologic substances in the pulmonary interstitium leads to an increase in lung elastic recoil, reduction in lung compliance, compression of microvasculature and inhibition of gas diffusion through the air-blood barrier. In such settings, perfusion is affected the most. Ventilation is reduced too, but not so severe as in obstructive lung diseases, and usually allows tachypnea to compensate blood gases abnormalities.

How lung volumes are changed in restrictive lung diseases?
1) Residual volume (RV) decreases due to an increased elastic recoil
2) Total lung capacity (TLC) decreases because of low RV and low VC (reduced compliance)
3) Forced vital capacity (FVC) moderately decreases because of extensive parenchymal fibrosis and preserved airway conductivity
4) Forced expiratory volume in 1 sec (FEV1) slightly-moderately decreases (similar to FVC)
5) FEV1 / FVC ratio remains normal or slightly increases [see explanation in 3) and 4)]
Therefore, TLC and FEV1/FVC are widely used in clinical practice for differentiation of obstructive and restrictive lung diseases.

ABGs in patients with restrictive lung diseases
Severe inhibition of perfusion along with relatively spared ventilation lead to severe hypoxemia. In such settings, tachypnea becomes a leading compensatory mechanism and a reason of PaCO2 reduction (hypocapnia).

Respiratory failure in patients with restrictive lung diseases
If hypoxemia falls below 60 mm Hg, respiratory failure ensues. But contrary to obstructive diseases, in restrictive diseases hypoxia is not associated with raise in carbon dioxide. In such patients hypocapnia and respiratory alkalosis usually persists, therefore the condition is named hypoxic respiratory failure. If respiratory failure worsens, concentration of carbon dioxide can turn from low to high. Hypercapnia in patients with restrictive lung disease is a grave sign implying an inability to maintain adequate alveolar ventilation.

I hope you found my explanations useful.

Good luck,

Dr. Y.