Diagnosis of acute respiratory failure

The symptoms of acute respiratory failure are varied and depend on the cause and the impact of blood gas disturbances on target organs - the lungs, heart, and nervous system. There are no specific symptoms of acute respiratory failure.

Clinical manifestations of acute respiratory failure

System	Symptoms
General condition	Weakness, sweating
Respiratory system	Tachypnea Bradypnea Apnea Decreased or absent breathing sounds Cyanosis Paradoxical breathing Flaring of the wings of the nose Grunting exhalation Wheezing
Cardiovascular system	Tachycardia Bradycardia Hypertension Hypotension Arrhythmia Paradoxical pulse Heart failure
CNS	Optic disc edema Respiratory encephalopathy Coma Asterixis

If a child exhibits one or more clinical signs, it is necessary to conduct a blood gas analysis, which allows not only to confirm the diagnosis of acute respiratory failure, but also to monitor the clinical development of the process. Blood gas analysis is the "gold standard" of intensive care: p _a O ₂, S _a O ₂, p _a CO ₂ and pH. Additionally, it is possible to measure carboxyhemoglobin (HbCO) and methemoglobin (MetHb). Blood for the study is taken from any part of the vascular system (venous, arterial, capillary), thereby obtaining various values for assessing oxygenation and ventilation.

Hypoxemia is a decrease in p _a O ₂, <60 mm Hg and S _a O ₂ <90% in the blood. The initial stage is characterized by tachypnea, tachycardia, moderate arterial hypertension, narrowing of the peripheral vessels; subsequently, bradycardia, arterial hypotension, cyanosis, impaired intellectual function, convulsions, disorientation, and coma develop. Mild hypoxemia is accompanied by moderate hypoventilation, impaired intellectual function and vision. Severe hypoxemia (p _a O ₂ <45 mm Hg) causes pulmonary hypertension, impaired cardiac output, myocardial and renal function (sodium retention), and CNS (headaches, somnolence, convulsions, encephalopathy), leading to anaerobic metabolism followed by the development of lactic acidosis.

Hypercapnia (p _a CO2 >60 mm Hg) also leads to impaired consciousness and heart rhythm, arterial hypertension. Early diagnosis and severity assessment depend on the results _of blood gas analysis.

The side effects of hypoxemia, hypercapnia, and lactic acidemia have synergistic or additive effects on other organs. Respiratory acidosis potentiates the hypertensive effect caused by hypoxemia and increases neurological symptoms.

Cyanosis is an important indicator of acute respiratory failure.

There are two types of cyanosis:

• central;
• peripheral.

Central cyanosis develops in respiratory pathology or in some congenital heart defects and manifests itself in hypoxemic hypoxia. Peripheral cyanosis is a consequence of hemodynamic problems (ischemic hypoxia). Cyanosis is absent in patients suffering from anemia, until severe hypoxemia occurs.

A general clinical and laboratory assessment is necessary, since the degree of respiratory distress does not always correlate with the degree of oxygenation and alveolar ventilation. Due to the various manifestations of acute respiratory failure in children, certain difficulties arise in diagnosis. For clinical and laboratory diagnosis of the development of acute respiratory failure, its timely and correct assessment is necessary.

Main criteria for the diagnosis of acute respiratory failure in children

Clinical	Laboratory
Tachypnea-bradypnea, apnea Paradoxical pulse Reduced or absent respiratory sounds Stridor, wheezing, grunting Marked retraction of the compliant areas of the chest using accessory respiratory muscles Cyanosis with the introduction of 40% oxygen (to exclude congenital heart defect, disturbances of consciousness of varying degrees	P a CO 2 <60 mm Hg with 60% oxygen administration (to rule out congenital heart defect) R a CO2. >60 mm Hg. PH <7.3 Vital capacity of the lungs <15 ml/kg Maximum inspiratory pressure <25 cm H2O,

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