Respiratory failure

Respiratory failure Is a condition in which a disturbance in the function of the respiratory system worsens gas exchange in the lungs and leads to hypoxemia (decrease in the partial pressure of oxygen in the arterial blood[PaO2]45 mmHg[6,0 кПа]). Distinguish hypoxemic insufficiency (without hypercapnia - partial, type 1) and hypoxemic hypercapnic (total, type 2).


1. Mechanisms of development of hypoxemia

1) inconsistency of alveolar ventilation to pulmonary perfusion:

  • a) reduction of alveolar ventilation (eg, due to atelectasis or filling of alveoli with fluid) with unchanged or slightly reduced pulmonary perfusion? decrease in the partial pressure of oxygen in the alveolar air? deteriorated oxygenation of blood flowing from the alveoli? in pulmonary veins well oxygenated blood, from areas of the lungs that are sufficiently ventilated mixed with worse oxygenated blood that flows from poorly ventilated areas of the lungs? decrease in partial pressure of oxygen in the pulmonary veins, left atrium, left ventricle and arteries of the great circle of blood circulation;

  • b) worsening of pulmonary perfusion - more often, due to pulmonary embolism or shock;

  • 2) intrapulmonary shunting of non-oxygenated blood - if the blood flow in the lung area is devoid of ventilation and gas exchange is retained (for example, due to airway obstruction or filling of the alveoli with liquid), then the neo-oxygenated blood flows from this site to the pulmonary veins, where it mixes with oxygenated blood flowing from enough ventilated alveoli. The greater the proportion of neo-oxygenated blood, the more pronounced hypoxemia and the weaker effect when applying oxygen therapy without using mechanical ventilation of the lungs with positive pressure;

    3) extrapulmonary bypass neo-oxygenated blood - a combination between the large and small circle of blood circulation (cyanotic heart defects and large vessels) lead to hypoxemia, weakly reacts to oxygen therapy;

    4) violation of alveolar-capillary diffusion, due to thickening of the air-blood barrier and deterioration of its permeability for oxygen caused by interstitial changes in the lungs;

    5) decrease in the partial pressure of oxygen in the respiratory gas mixture - staying at a high altitude (lowering the atmospheric pressure).

    2. Consequences of hypoxia

  • 1) tissue hypoxia? anaerobic metabolism? lactacidosis? cell death? multi-organ failure? death;

  • 2) compensatory reactions (temporary, disappear with prolonged hypoxemia) - tachycardia, increased blood pressure, increased cardiac output, hyperventilation;

  • 3) pulmonary hypertension - due to reflex spasm of pulmonary arterioles and an increase in their resistance; constant, due to reconstruction of the walls of the pulmonary vessels;

  • 4) right ventricular heart failure - overload, hypertrophy and insufficiency of the right throat due to secondary pulmonary hypertension, which occurs in response to hypoxemia caused by respiratory system disease ("pulmonary heart");

  • 5) secondary erythrocytosis (polycythemia) - chronic hypoxemia activates the synthesis of erythropoietin in the kidneys and enhances erythropoiesis;

  • 6) fingers in the form of tympanic sticks and hypertrophic osteoarthropathy.

  • hypercapnia

    1. Mechanism of hypercapnia development: alveolar hypoventilation plays a decisive role, since the aerogematic barrier capacity for CO2 in? 20 times better than O2; in this regard, thickening or deterioration of the permeability of this barrier and the reduction of pulmonary perfusion do not have such a significant effect on the exchange of CO2 between air and blood, as in the case of O2.

    2. The reasons for hypoventilation

    1) increased load on the respiratory system (respiratory work):

  • a) increase in airway resistance for air movement - violation of upper airway patency (foreign body, laryngeal edema, loss of consciousness), lower airway obstruction (bronchial smooth muscle spasm and mucosal edema - COPD, asthma, obstruction of the bronchi by secretions or swelling) , obstructive sleep apnea syndrome;

  • b) decreased lung compliance - filling of the alveoli with fluid (pulmonary edema, intra-alveolar bleeding), pneumonia, interstitial lung diseases, atelectasis, dynamic hyperinflation (mainly in COPD), lung contusion (extravasation of blood); fluid in the pleural cavity (cavities), pneumothorax;

  • c) decreased compliance of the chest - significant obesity, high diaphragm standing (bloating, ascites, paresis of the diaphragm); deformities, injuries and tumors of the chest wall;

  • d) forced increase in minute ventilation (relative hypoventilation) - shock, hypovolemia, sepsis, pulmonary embolism;

  • 2) violation of the function of the respiratory muscles and nervous system:

  • a) a decrease in the activity of the respiratory center - an overdose of drugs (opioids and hypnotics) or drugs, damage to the brainstem, sleep apnea of ​​central etiology, myxedemaemia coma;

  • b) disorders of nervous and neuromuscular conduction - damage to the diaphragmatic nerves, trauma of the cervical or thoracic spinal cord, Guillain-Barre syndrome, myasthenic crises, tetanus, botulinum toxin poisoning, muscle relaxants, acute intermittent porphyria, amyotrophic lateral sclerosis, multiple sclerosis;

  • c) weakness of the respiratory muscles - overload (increase in the work of breathing), electrolyte disorders (hypokalemia, hypomagnesemia, hypophosphatemia), acidosis, hypotrophy, hypoxia, shock, muscle diseases.

  • 3. Consequences of hypercapnia

  • 1) respiratory acidosis;

  • 2) headache and impaired consciousness - confusion, pathological somnolence and hypercapnia coma - is associated with the expansion of cerebral vessels and increased intracranial pressure;

  • 3) respiratory drive, depending on hypoxemia - chronic respiratory failure and hypercapnia lead to a decrease in the sensitivity of the respiratory center of the medulla oblongata and the bridge to an increase in the partial pressure of CO2. In such a situation, the respiratory center is stimulated mainly by pulses from chemoreceptors sensitive to PaO2; which are in the dormant glomeruli and the arch of the aorta. In this case, too aggressive oxygen therapy and increased PaO2 reduce the activity of the respiratory center and lead to hypoventilation and hypercalcic respiratory failure, which leads to coma.