Respiratory Insufficiency

Respiratory insufficiency (RI), also referred to as respiratory failure, is a condition in which the respiratory system is unable to ensure adequate gas exchange. The disorder may affect all lung functions, ventilation, diffusion, and perfusion. The consequence is hypercapnia (insufficient elimination of carbon dioxide from the blood), hypoxemia (insufficient oxygen content in arterial blood), or a combination of both.

Epidemiology

Epidemiological data indicate that the incidence of acute respiratory insufficiency according to current criteria is approximately 8 cases per 100,000 population. Chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), bronchial asthma, and others, are very common in the population and lead to the development of chronic respiratory insufficiency in approximately 5% of cases.

Figure A shows the location of the lungs, airways, diaphragm, rib cage, pulmonary arteries, brain, and spinal cord in the body. Figure B shows the major conditions that cause respiratory failure

Classification

Respiratory insufficiency can be classified according to several criteria.

According to the speed of onset:

• Acute – immediate compensatory mechanisms are activated, such as hyperventilation, tachypnea, and tachycardia, typically caused by conditions such as ARDS.
• Chronic – characterized by long-term compensatory mechanisms, including renal compensation of acid–base balance and polycythemia compensating for hypoxia, which is typical of COPD, bronchial asthma, or pulmonary fibrosis.

According to manifestation:

• Latent – a decrease in arterial oxygen partial pressure (pO₂) occurs only during physical exertion.
• Manifest – a decrease in pO₂ and a possible increase in pCO₂ occur even at rest.

According to blood gas abnormalities:

• Hypoxemic respiratory insufficiency (Type I, partial) – characterized by decreased pO₂, while pCO₂ may be decreased due to hyperventilation, leading to respiratory alkalosis. This type is typical of acute respiratory insufficiency, with PaO₂ < 7.3–7.9 kPa, PaCO₂ < 5.3 kPa, and an increased alveolar–arterial oxygen gradient (A–aDO₂).
• Hypoxemic–hypercapnic respiratory insufficiency (Type II, global) – characterized by decreased pO₂ and increased pCO₂ due to hypoventilation, which may result in respiratory acidosis. This type is typical of chronic conditions such as COPD or idiopathic pulmonary fibrosis and may be compensated or decompensated. PaO₂ values are below 7.3–7.9 kPa, PaCO₂ exceeds 6.6 kPa, and A–aDO₂ may be normal or increased.

Etiology

The etiology of respiratory insufficiency includes two main groups of causes. The first group is pulmonary failure, which may result from diseases of the airways, alveoli, alveolo-capillary membrane, or pulmonary circulation. The second group comprises extrapulmonary failure, in which the disorder lies in dysfunction of the respiratory center, medulla oblongata, respiratory muscles or their innervation, or in diseases of the chest wall.

Pathophysiology

The pathophysiology of respiratory insufficiency includes mechanisms leading to hypercapnia and hypoxemia.

Mechanisms leading to the development of hypercapnia

Mechanism	Causes	Examples
Reduced alveolar ventilation	Central nervous system depression	Unconsciousness, status epilepticus, narcotic effects
	Peripheral nervous system disorders	Cervical spine injury, Respiratory muscle failure or fatigue
	Respiratory muscle failure or fatigue	Muscular dystrophies, shock states, and increased work of breathing
	Upper airway obstruction	Laryngitis, foreign body, tracheomalacia
	Reduced lung compliance	Pulmonary edema, fibrosis
	Increased chest wall compliance	Chest trauma
	Disrupted pleural space	Pneumothorax
Increased dead space ventilation	Reduced pulmonary circulation	Pulmonary hypertension, reduced cardiac output
	Alveolar overdistension	Asthma
Increased CO₂ production	Increased metabolism	Burns
	Altered respiratory quotient	High glucose intake

Mechanisms leading to the development of hypoxemia

Mechanism	Causes	Examples
Pulmonary shunt with increased pulmonary vascular resistance (PVR)	Diffuse intra-alveolar fluid, pulmonary vascular obliteration	ARDS
Pulmonary shunt without increased PVR	Local intra-alveolar fluid	Lobar pneumonia
Reduced V/Q ratio with increased PVR	Bronchospasm with pulmonary hypertension	Cardiogenic pulmonary edema
Intracardiac shunt with increased PVR	Right-to-left shunt with pulmonary hypertension	Endocardial defects
Intracardiac shunt without increased PVR	Right-to-left shunt	Pulmonary stenosis with ventricular septal defect
Hypoventilation	Reduced alveolar ventilation	Upper airway obstruction
Diffusion impairment	Interstitial thickening	Fibrosis
Reduced mixed venous oxygen saturation	Increased oxygen extraction	Cardiogenic shock

Clinical picture

The clinical picture of respiratory insufficiency includes tachypnea and dyspnea with active use of accessory respiratory muscles. Other manifestations include tachycardia and cyanosis. Auscultation often reveals diminished or absent breath sounds. Psychological and neurological symptoms may also occur, such as anxiety, agitation, and quantitative impairment of consciousness.

Hypoxemia stimulates peripheral chemoreceptors, leading to hyperventilation, while sympathetic activation causes tachycardia, increased sweating, anxiety, and agitation. With further decline in oxygen levels, neurological symptoms develop, including reduced mental performance, confusion, and potential circulatory instability with fluctuations in blood pressure and heart rate. As hypoxemia progresses, ventilation also fails, leading to hypercapnia and central nervous system depression.

Hypercapnia manifests as changes in consciousness, somnolence may be replaced by restlessness, tremor, and headache. In severe hypercapnia, intracranial hypertension may develop, and with further increases in pCO₂, coma ensues. Central cyanosis occurs particularly in chronic patients with polycythemia.

Diagnostics

Diagnosis of respiratory insufficiency includes assessment of acid–base balance and arterial blood gases. In the early phase, respiratory acidosis with low pH and elevated pCO₂ is present; later, hypoxemia with decreased PaO₂ develops.

Medical history plays a crucial role, focusing on the circumstances of dyspnea onset, possible intoxication or infection, and the state of consciousness, which may be significantly impaired in chronic patients with decompensated hypercapnia. Physical examination may reveal various pulmonary auscultatory findings depending on the underlying disease, as well as cyanosis.

Imaging methods such as chest X-ray or CT often demonstrate significant changes consistent with the primary disease. Depending on the clinical context, spirometry, ECG, echocardiography, and other supplementary tests may be performed.

Therapy

Treatment of respiratory insufficiency is primarily aimed at managing the underlying disease. Simultaneously, hypoxia and hypercapnia must be corrected by administering warmed and humidified oxygen via a mask, nasal cannula, or endotracheal tube. It is also necessary to ensure adequate cardiac output, maintain oxygen saturation (SpO₂) above 90%, and keep hematocrit above 30%.

Therapy also includes support of lung tissue repair, encompassing adequate nutrition, minimization of oxygen toxicity by administering the lowest possible fraction of inspired oxygen (FiO₂) to maintain normal PaO₂ values, and prevention or elimination of nosocomial infections.

The most common causes of respiratory failure in children

The most common causes of respiratory failure in children include a wide spectrum of diseases and conditions, which can be divided into several main groups:

Group of causes	Examples
Central nervous system	Craniocerebral trauma, intracranial hemorrhage, intoxication
Neuromuscular	Spinal cord injury, Guillain–Barré syndrome, myasthenia gravis, phrenic nerve paresis, muscular dystrophies/atrophies, respiratory muscle fatigue, cachexia
Upper and lower respiratory tract	Epiglottitis, laryngitis, foreign body aspiration, asthma, bronchiolitis
Pulmonary	Pneumonia, pulmonary edema, ARDS, pulmonary embolism, persistent pulmonary hypertension
Pleural	Pneumothorax, hemothorax, chylothorax

References

• Kumar V, Abbas AK, Aster JC. Robbins and Cotran Pathologic Basis of Disease. Elsevier.
• Hammer GD, McPhee SJ (eds.). Pathophysiology of Disease: An Introduction to Clinical Medicine. McGraw-Hill Education, 2014.
• Maruna P. Examination Tests from Pathological Physiology. Karolinum, 2015.