Respiratory Distress and Failure

1. Respiratory distress. A compensated state in which normal gas exchange is maintained at the expense of increased work of breathing. Typically this manifests as tachypnea and increased work of breathing. When adequate oxygenation, ventilation, or both cannot be maintained, respiratory failure ensues. Ventilation is a complex physiologic process, primarily controlled by carbon dioxide. Other influences come from peripheral chemoreceptors that sense changes in blood pH, carbon dioxide, and Po2. Pulmonary stretch receptors, irritant receptors, and J receptors can all influence ventilation in certain circumstances.

a. Dyspnea. Subjective sensation of difficult, labored, and uncomfortable breathing. Children may not be able to report or describe dyspnea. There are pulmonary and nonpul-monary causes; in children, most causes are pulmonary.

b. Tachypnea. An objective measurement of increased respiratory rate for age. Healthy newborns typically breathe 24-40 times per minute. Normal respiratory rate decreases with age to adult normal value of 14-20 breaths per minute.

2. Respiratory failure. Inability of respiratory system to supply body with adequate oxygen and to remove carbon dioxide. Can be divided into two categories: failure to oxygenate (hypoxemic) and failure to ventilate (hypoventilatory). Both can be seen in pediatric patients and may occur together. Ventilatory support is indicated when adequate gas exchange cannot be independently achieved or maintained. a. Hypoxemia and hypoxemic respiratory failure i. Findings. Hypoxemia describes a decreased oxygen tension in the blood (Pao2). Oxygenation can be determined by measurement of pulse oximetry (Spo2) or partial pressure of oxygen in arterial blood (Pao2). By evaluating PaO2 in context of fraction of inspired oxygen (Fio2) employed, objective criteria for hypoxemic respiratory failure can be established. Ratio of Pao2 to Fio2 (P/F ratio) is used to characterize hypoxemia. P/F ratio < 200 is consistent with ARDS, whereas a ratio between 200 and 300 is consistent with acute lung injury. Patients with P/F ratio < 300 or Spo2 < 90-93% (in absence of cyan-otic heart disease) require additional support, especially if they demonstrate signs of inadequate oxygen delivery (eg, tachycardia, metabolic acidosis, or end-organ dysfunction). Although these patients may be managed initially with high oxygen delivery systems, their disease may progress to a point at which ventilatory support is required. Because of their physiologic instability and potential need for advanced therapies, these patients should be closely monitored in a pediatric intensive care unit. Worsening of respiratory status necessitates prompt intubation and ventilatory support. Prototype disease for hypoxemic respiratory failure is ARDS, in which high shunt fraction leads to refractory hypoxemia.

ii. Pulmonary causes. Absolute (true) shunt: Blood passes from right to left heart without being exposed to alveolar oxygen; no response is shown to increased Fio2; examples include capillary shunting (eg, ARDS, pneumonia, atelectasis) and anatomic shunting (eg, congenital heart defect, arteriovenous malformations). Relative shunt (venous admixture): Ventilation-perfusion (V/Q) mismatch (perfusion in excess of ventilation); for example, asthma. Hypoventilation: Carbon dioxide replaces oxygen in lungs. Diffusion defects: Alveolar-capillary membrane can be widened significantly without resultant hypoxemia. If it thickens (eg, fibrosis), diffusion may be reduced to the extent of resulting hypoxemia. This is unusual. In most interstitial lung diseases (eg, interstitial pneumonitis), hypoxemia is due to V/Q mismatch rather than diffusion defects. iii. Nonpulmonary causes. Decrease in cardiac index. Decrease in oxygen-carrying capacity (hemoglobin/ RBCs). Increase in oxygen consumption (Vo2).

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