Test: Spirometry, DLco, Alveolar-Arteriolar Gradient & Types of Respiratory Failure- 2 - NEET PG MCQ

CT chest offers the most dependable perspective on mediastinal anatomy.

• The primary characteristic is reduced opacification of central venous structures, accompanied by notable collateral venous circulation.
• Following this, an endobronchial or ultrasound-guided biopsy may be performed to determine the underlying cause.
• The diagnosis of superior vena cava syndrome (SVCS) is primarily clinical.
• A chest X-ray (CXR) reveals superior mediastinal widening, with pleural effusion occurring in 25% of cases.
• The clinical sign indicating increased facial venous congestion when raising the arms above head level is referred to as the Pemberton sign.

Methemoglobin exhibits such a strong affinity for oxygen that it virtually prevents oxygen delivery to tissues, resulting in central cyanosis.

• Levels of 50-60% are typically lethal.
• All other causes result in peripheral cyanosis.

The crescendo-decrescendo breathing pattern is referred to as Cheyne-Stokes breathing. It is defined by:

• Hyperventilation alternating with periods of apnea.
• Also known as Central Apnea.

This pattern arises from prolonged circulation in congestive heart failure (CHF), which causes a delay between pulmonary capillaries and carotid chemoreceptors. In contrast, obstructive sleep apnea does not involve hyperventilation and is therefore excluded.

The presence of morbid obesity alongside respiratory distress and orthopnea suggests that congestive heart failure could be a likely cause. The patient exhibits low pO₂ and low PCO₂, indicating the onset of type 1 respiratory failure. This alveolar flooding is a result of increased pulmonary microvascular pressures. The reduced CO₂ levels can be attributed to the patient’s hyperventilation. For the treatment of type I respiratory failure, it is advised that the patient receives low tidal ventilation.

• Mechanical ventilation may result in volutrauma and is therefore not recommended for these individuals.
• Choice B is applicable in cases of type II respiratory failure.
• Endotracheal intubation increases the effort required for breathing in type II respiratory failure.

As such, type II respiratory failure is treated with non-invasive ventilation. In Choice C, intravenous diuretics are necessary for managing pulmonary oedema, but digoxin is not utilised in the acute management of CHF in adults. Choice D is appropriate for type II respiratory failure.

Type 4 respiratory failure arises from inadequate blood flow to the respiratory muscles in individuals experiencing shock.

• Under normal circumstances, the respiratory muscles use less than 5% of the total cardiac output and oxygen supply.
• However, in shock, patients may have as much as 40% of their cardiac output directed towards these muscles.
• Utilising intubation and ventilator support facilitates the redistribution of cardiac output away from the respiratory muscles.

Non-invasive ventilation with a snugly fitting face mask is employed in the treatment of type 2 respiratory failure, such as during exacerbations of COPD.

• Increased resistive loads, such as bronchospasm in COPD.
• Loads resulting from decreased lung compliance, for example, alveolar oedema, atelectasis, and intrinsic positive end-expiratory pressure.
• Reduced central nervous system drive to breathe due to factors like drug overdose, brainstem injury, sleep-disordered breathing, and hypothyroidism.
• Decreased strength may stem from impaired neuromuscular transmission, as seen in myasthenia gravis, Guillain-Barre syndrome, amyotrophic lateral sclerosis, or phrenic nerve injury.
• Weakness of respiratory muscles can occur due to myopathy, electrolyte imbalances, or fatigue.
• Loads caused by decreased chest wall compliance, such as pneumothorax, pleural effusion, and abdominal distension, along with those arising from increased minute ventilation needs, for instance, pulmonary embolism with heightened dead space fraction or sepsis.

• issues within the central nervous system
• disruption of neuromuscular transmission
• mechanical problems with the ribcage
• fatigue of the respiratory muscles

• Reduced FRC
• Supine position/obesity/ascites
• Anaesthesia
• Upper abdominal incision
• Airway secretions

• Reposition the patient every 1-2 hours
• Administer chest physiotherapy
• Encourage incentive spirometry
• Manage incisional pain (which may involve epidural anaesthesia or patient-controlled analgesia)
• Ventilate at a 45-degree angle
• Drain any ascites
• Avoid overhydration

The A-a gradient rises in type I respiratory failure because it impacts only paO₂.
In contrast, the A-a gradient remains normal in type II respiratory failure since it reduces both pAO₂ and paO₂.

Neuromuscular disorders that may lead to alveolar hypoventilation encompass:

• myasthenia gravis
• amyotrophic lateral sclerosis
• Guillain-Barre syndrome
• muscular dystrophy

Individuals suffering from neuromuscular conditions exhibit rapid, shallow breathing due to:

• severe muscle weakness
• abnormal motor neuron activity

The central respiratory drive remains intact in those with neuromuscular disorders. Consequently, hypoventilation arises from weakness in the respiratory muscles.

Paradoxical breathing involves movements where the chest wall contracts during inhalation and expands during exhalation, opposite to the typical pattern. This can occur in cases of crush injuries to the chest, resulting in fractured ribs and sternum, which can cause significant paradoxical breathing. It may also be observed in children experiencing respiratory distress from various causes, leading to the retraction of the intercostal spaces during inhalation.

Individuals with chronic airway obstruction may also demonstrate the retraction of the lower ribs during inhalation, due to the altered function of a flattened and depressed diaphragm.

Hyperventilation results in the expulsion of CO₂ from the body, causing respiratory alkalosis. The H⁺ ions on the buffer base are then utilised to counteract this alkalosis. This process creates several unoccupied sites on the buffer base, which are subsequently filled by calcium. Given that calcium exists in two states—bound and ionised—an increase in calcium binding to these vacant protein sites leads to a reduction in the level of ionised calcium. This drop causes tetany. Additionally, somnolence or drowsiness is characteristic of carbon dioxide narcosis, which occurs alongside respiratory acidosis or hypoventilation.

Polio and M. Gravis can result in diaphragmatic paralysis. In the case of acute intermittent porphyria, the clinical presentation of acute episodes includes:

• Vomiting
• Hypertension and tachycardia
• Severe abdominal pain (with an incidence estimated between 85% and 95%)
• Peripheral neuropathy accompanied by muscle weakness (42% to 68%)

Respiratory failure is less frequent and less recognised (9% to 20%). The precise mechanism by which these signs and symptoms arise is still unknown.