Test: Spirometry, DLco, Alveolar-Arteriolar Gradient & Types of Respiratory Failure- 1 - NEET PG MCQ

The timed vital capacity ratio of FEV1/FVC decreases in obstructive lung disease and returns to normal levels in restrictive lung disease. Meanwhile, FEV1 is diminished in both restrictive and obstructive lung conditions.

The image displays the compliance curve of the lungs, with curve A indicating enhanced compliance, a characteristic of emphysema. The options B, C, and D demonstrate decreased compliance and align with curve B.

• In central causes of hypoventilation A-a gradient is normal. This is because pAO₂, and paO₂, reduce by the same magnitude. Minute ventilation is reduced.
• In pulmonary causes of hypoventilation A-a gradient is increased. Minute ventilation is normal to increased.
• Choice B, C and D will be affected in similar fashion in both types of hypoventilation.

Remember in acute severe asthma, hypoventilation leads to normal A-a gradient.

After a lobectomy, as there is less remaining lung tissue, various parameters such as vital capacity, residual volume, and closing volume will decrease. Consequently, due to the hypoxic stimulus, patients who have undergone lobectomy will exhibit rapid, shallow breathing.
This change will result in an increase in dead space ventilation.

The FEV1/FVC ratio for the patient is reduced, suggesting obstructive airway disease. Coal workers' pneumoconiosis is linked to the impact of coal dust on alveolar macrophages, resulting in the onset of chronic bronchitis and COPD. Many individuals here incorrectly respond with pulmonary fibrosis.
Interpretation of Spirometry Data

DLCO is elevated in Goodpasture syndrome due to the damage to the basement membrane, which enhances the likelihood of CO diffusion across fewer anatomical layers. In contrast, DLCO is reduced in pulmonary artery hypertension because fibrosis in the pulmonary vessels diminishes the diffusion of CO through the anatomical layers.
Causes of increased DL_CO:

• CHF
• Goodpasture syndrome
• Asthma
• Polycythaemia

All expiratory parameters are diminished in the provided data, with a timed vital capacity of 29%. The FEV1/FVC ratio is lowered in cases of obstructive airway disease, accompanied by a decrease in peak expiratory flow rates.

• As a result of air trapping in asthma, the DLco may either remain normal or show an increase.

Points supporting this include:

• The occurrence of an industrial accident involving hyperdynamic cardio vascular symptoms in a drowsy patient who exhibits normal oxygen saturation.
• Cherry red lips are a finding observed post-mortem and are not typically seen before death.
• A standard pulse oximeter is ineffective for diagnosing carbon monoxide poisoning, as individuals affected may display a normal oxygen saturation reading. This occurs because carboxyhaemoglobin is incorrectly identified as oxyhaemoglobin.
• Workers in environments such as pulp mills, steel foundries, and facilities producing formaldehyde or coke are at risk of exposure, as are firefighters and those operating indoors with combustion engines or flammable gases.

As a result, SaO₂ readings can appear falsely normal. Additionally, hyperventilation accounts for low pCO₂.

In central hypoventilation, both pAO₂ and paO₂ are diminished, resulting in a typical alveolar-arteriolar gradient.

• It is important to note that the alveolar-arterial O₂ gradient is elevated in cases of alveolar hypoventilation.
• Conversely, the alveolar-arterial O₂ gradient remains normal in central hypoventilation.

Since the pH has decreased and CO₂ has risen, the main alteration in the patient is respiratory compromise.

• The rise in CO₂ will cause an increase in H₂CO₃, resulting in the generation of H⁺.
• The elevated H⁺ levels will contribute to acidosis, prompting the compensation mechanism to activate.
• This compensation involves an increase in HCO₃ to counterbalance the heightened H⁺ concentration.

Now, as the HCO₃ level has risen (Normal = 22-26 meq), it indicates that compensation has commenced. However, since the pH has not returned to the normal range and remains at 7.3, it suggests that compensation is incomplete. The final conclusion is that the patient is experiencing partially compensated respiratory acidosis.

The existence of reduced TLC indicates a restrictive pattern, which is further validated by a normal FEV1/VC ratio.

• Options A and C lead to obstructive airway disease.
• ABPA results in central bronchiectasis and is classified as a suppurative lung disease.

ABG indicates significant hypoxia combined with hypercapnia and acidosis, which points to type 2 respiratory failure. Both ARDS and acute asthma are characterised by type 1 failure, so these can be excluded.

• This leaves us with options A and C to consider.
• Routine presentation of interstitial pneumonitis typically does not exhibit such low oxygen levels.
• However, an acute exacerbation of chronic bronchitis will certainly show low oxygen values.

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Pulmonary plethysmographs are frequently utilised to evaluate the functional residual capacity (FRC) of the lungs—this refers to the volume within the lungs when the respiratory muscles are at rest—and the total lung capacity. The contrast between fully inflated and deflated lungs can be employed to identify diseases and restrictions in the airway passages.

• An obstructive disease will demonstrate an increased FRC as certain airways fail to empty properly.
• A restrictive disease will reveal a decreased FRC.

Body plethysmography is especially suitable for patients with air spaces that do not connect with the bronchial tree; in these cases, helium dilution would yield an inaccurately low measurement. It is important not to confuse this with impedance plethysmography, which is a non-invasive technique used to detect venous thrombosis in specific areas of the body.

In restrictive lung disease, the involvement of the parenchyma results in pulmonary fibrosis, making it challenging to inflate the lungs, which consequently reduces lung compliance.
The FEV1/FVC ratio is elevated in restrictive lung disease because both the numerator and denominator in this ratio are diminished, with the FVC decreasing disproportionately.

In obstructive lung disease, the FEV1 is diminished because of the obstruction preventing air from exiting the lungs. Therefore, the FEV1/FVC ratio will also be lower. Specifically, in this case, 1.3/3.1 equates to roughly 40%, compared to a normal value of over 80%. More precisely, as per the National Institute for Clinical Excellence, a diagnosis of COPD is confirmed when the FEV1/FVC ratio falls below 60%. According to the criteria set by the European Respiratory Society (ERS), a COPD diagnosis is established if the patient's FEV1% is under 88% of the predicted value for men or below 89% for women. In restrictive lung disease, both FEV1 and FVC are similarly reduced due to factors like fibrosis or other lung conditions (rather than obstructive issues). Consequently, the FEV1/FVC ratio should typically be within normal limits or may even be elevated.

Alveolar arteriolar gradient = pAO₂ - paO₂

• Options A, C, and D will only affect paO₂, resulting in an increase in the gradient.
• A greater gradient indicates a more severe condition, necessitating ventilator assistance.

The reasons for an increased alveolar arteriolar mismatch include:

• V/Q Mismatch (e.g., pneumonia, congestive heart failure, acute respiratory distress syndrome, atelectasis)
• Shunt (e.g., patent foramen ovale, atrial septal defect, pulmonary embolism, pulmonary arteriovenous malformations)
• Alveolar Hypoventilation (e.g., interstitial lung disease, environmental lung disease)

It is important to note that hypoventilation resulting from central nervous system diseases or neuromuscular disorders will diminish the ventilatory drive, leading to a decrease in both pAO₂ and paO₂.

Vital capacity is a sum of IRV + TV+ ERV and all these lung volumes are reduced in restrictive lung disease.

Sarcoidosis impacts lung parenchyma and may result in lung fibrosis. This condition can cause the emergence of a restrictive pattern. It is important to note that if it leads to lymphadenopathy compressing the airway, it may also produce an obstructive pattern.