Most infants and children are healthy, however, when they do have serious illness or injury, early assessment and intervention is critical to assure a good outcome. Cardiopulmonary arrest in the pediatrie age group is usually not a sudden event but is the result of a progressive deterioration of illness or injury that leads to respiratory or circulatory compromise. Should a cardiopulmonary arrest occur, early resuscitation may have some effect on mortality, but in general the outcomes from these events in the prehospital phase, as well as in the medical office, emergency department, or inpatient setting, are poor.1'3
few clinicians have difficulty recognizing the infant or child who is in an extreme state with respiratory or circulatory failure. If one pictures the child on a roller coaster at the top of the rise about to accelerate on the steep slope, one can see that once the cars start to accelerate downward, there is no turning back. This is analogous to shock and respiratory failure. Once the infant or child can no longer compensate for deficiencies in ventilation, oxygenation, or perfusion, there is a rapid progression to cardiopulmonary failure and cardiac arrest. Clinicians who see ill and injured children must, therefore, be able to recognize the patient who is in a compensated state and provide early intervention to improve outcome.4
RESPIRATORY DISTRESS AND FAILURE
Infants and children normally breath with a minimum of effort. Respiratory rates vary with age; an infant may breath 40 breaths per minute, while a 1 year old breaths 25 breaths per minute, and a 10 year old only 18 breaths per minute (Table). Although these rates may increase with anxiety, rapid respiratory rates always require complete assessment. Rates of 60 breaths or more per minute may be a sign of severe distress. In young iniants, the diaphragm is the major muscle of respiration; thus, abdominal excursions should be observed and the rate counted for at least 30 seconds. In older children, the chest rise may also be observed.5
The tidal volume remains constant throughout life at 6 to 8 mL/kg. The minute ventilation may be assessed by observing the abdominal excursion or chest rise, listening in the axilla for breath sounds, and assessing the respiratory rate.
Minute Ventilation = Tidal Volume × Respiratory Rate
If the tidal volume is reduced so that the compensatory increase in respiratory rate does not provide sufficient minute ventilation for adequate gas exchange or the patient can no longer sustain the increased work of breathing, respiratory failure will ensue.
A child in respiratory distress may demonstrate signs of increased work in breathing, including retractions in the intercostal, substemal, and supraclavicular areas; nasal flaring; and use of the accessory muscles in the neck (Figure 1 ) . Supraclavicular retractions may be an ominous sign, as they are often associated with airway obstruction. The presence of abnormal respiratory sounds are due to turbulent air passing through a narrowed airway. Remember that resistance to flow through a hollow tube is inversely proportional to the radius of the lumen of the tube to the fourth power. Thus, the smaller the airway the more resistance to flow that will be generated by even small changes in the radius due to the pressure of edema, secretions, or foreign bodies. The nature of the sounds produced is dependent on the location of the narrowing in the airway. Gurgling and stridor come from the upper airway, ronchi and wheezing from the lower airway. If no audible sounds are evident and stethoscopic breath sounds are absent or decreased, the child's airway may be totally obstructed and respiratory arrest may be imminent. Grunting is caused by turbulent air coming in contact with a partially closed glottis. Patients who exhibit grunting are creating positive end expiratory pressure by generating a \alsalva maneuver during respiration that results in partial obstruction of the upper airway.
The inspiratory to expiratory ratio should also be observed. In most patients this is approximately one. Prolonged expirations are most often seen with reactive airway disease.
Signs of poor oxygénation include alterations in mental status, head bobbing, and change in skin color. Cyanosis is often a late sign and occurs when there are at least 5 grams of unsaturated hemoglobin per deciliter of blood in the circulation. Before this occurs, the child may first appear dusky or pale. If the child is anemic, cyanosis may not be evident even though the oxygen saturation is low. Oximetry is a means of rapidly assessing oxygen saturation.
Vital Signs by Age
Respiratory failure is defined as a clinical state in which there is either inadequate oxygenation of the blood or a failure in the elimination of carbon dioxide. This may be due to intrinsic lung disease, inadequate respiratory effort due to intracranial pathology, or heart failure. Patients in respiratory failure show the signs of respiratory distress noted above, particularly altered mental status and poor skin color or cyanosis. Measurements of oxygen saturation or arterial blood gases show either hypoxia or hypercapnia.
In emergency situations, assessment of the child's respiratory status and intervention often occur simultaneously. Thus, if respiratory distress is evident, patients must be given the highest concentration of oxygen that is possible to deliver, often while monitoring oxygen saturation. Never force a child to use an airway adjunct, as this may cause increased anxiety and distress. One must immediately determine if the patient has a clear enough airway to be maintained with simple interventions, such as oxygen delivered by facial blowing (blow-by), by mask, or by nasal prongs. If not, more advanced bag-valve-mask ventilation or endotracheal intubation will be necessary. These latter forms of airway support are reserved for patients who need assisted ventilation, protection of their airway, or hyperventilation. All patients with respiratory distress should be placed on a cardiac monitor for frequent assessment of their cardiac status.
Recognition of Impaired Perfusion
Shock is a clinical state characterized by a failure to supply sufficient oxygen and metabolic substrate to meet the metabolic demands of the tissues. There may be an increased consumption of substrate or poor perfusion of the tissues. There are many etiologies of shock; hypovolemia from trauma, vomiting, and diarrhea is the most common cause in children.6 Shock leads to metabolic acidosis and cell death.
Figure 1. Picture of an infant in respiratory distress. Note the retractions.
Shock may be classified as compensated, decompensated, or irreversible. Infants and children have an enormous capacity to compensate for hemodynamic changes and cardiovascular instability. Their hearts and blood vessels are generally healthy and can respond to volume changes by increases in peripheral vascular resistance and heart rate. The cardiac output, and thus blood pressure, may be maintained by these compensatory mechanisms. The diastolic pressure may also rise, causing a narrowed pulse pressure which is clinically apparent as a "thready" peripheral pulse. Compensated shock is present when the child shows clinical signs of shock and is normotensive. If the patient's blood pressure falls below 70 mmHg, decompensated shock is present. Irreversible shock is accompanied by multiple end organ failure due to prolonged poor perfusion. This is a retrospective diagnosis, as it always leads to death.
The assessment of a child in shock includes general appearance, heart rate, the character of the pulses, skin signs, the capillary refill time, and blood pressure. The most common pitfall in this assessment of infants and children is relying solely on blood pressure levels as a measure of circulatory status. The heart rate is often the first parameter that changes when there is absolute or relative volume depletion. Sinus tachycardia to rates of 200 are not uncommon; rates of 160 beats per minute or higher, however, require careful assessment. This may be accompanied by diminished or thready peripheral pulses, and the child may appear pale, with cool extremities. A temperature differential may be noted between the proximal and distal portions of the limbs. The palms may be cool and clammy, and the capillary refill time will exceed 2 seconds. There may also be altered mental status with lethargy, irritability, or coma. Children may remain in compensated shock until one fourth to one third of their circulating blood volume is depleted.7 When cardiac output drops, the child will decompensate and the blood pressure will fall. Children in decompensated states will almost certainly have altered mental status and their urine output will decrease to less than 1 cc/kg/hr. Failure of the child to recognize parents or caretakers is a poor clinical sign.
Figure 2. Placement of an intraosseous needle. A bone marrow needle with a stylet or one of several commercially available intraosseous needles may be used for this procedure. Reprinted with permission from Seidel JS and Henderson DP.5
As with respiratory distress, clinical assessment and intervention often proceed together. After attention is given to proper ventilation and oxygenation, the goal of intervention should be to restore a normal circulating blood volume. The largest and most accessible vein should be cannulated as soon as possible. One should start by attempting cannulation of a peripheral vein on the scalp, arm, hand, leg, or foot. After a few unsuccessful attempts or several minutes have expired, central venous access should be attempted via the femoral or jugular veins. The clinical status of the patient will determine the site used.8 The intraosseous approach to vascular access provides a quick lifeline when other approaches are unsuccessful. The needle (bone marrow, spinal, or intraosseous) should be positioned two finger breadths ( 1 to 3 cm) below the tibial tubercle on the medial aspect of the tibia. It should be placed perpendicular to the bone and inserted toward the midline (Figure 2). Once in the bone marrow, a fluid bolus is infused using a large syringe attached to the needle. A stop cock attachment is preferred to avoid leakage of the fluid, which must be pushed in under a good deal of pressure.
The treatment for most causes of shock is fluid administration.9 Boluses of isotonic crystalloid (20 mL/kg) should be infused as fast as possible by whatever access is available. Heart rate and other signs of shock should be reassessed after each fluid bolus is given. Patients with trauma who do not respond to several fluid boluses (up to 50 to 60 mL/kg of fluid) will require blood transfusions and may need immediate operative intervention to control the loss of blood. If the patient has underlying cardiac disease, poor perfusion may be due to fluid overload and thus fluid boluses should be given more cautiously. If rales and signs of congestive heart failure are present, infusions of fluid should be reduced.
The rapid assessment of the infant and child in respiratory distress and failure or shock, with the simultaneous institution of critical interventions, is necessary to improve outcomes in critically ill or injured children.
1 . Eisenberg M, Bergner L, Halberem A. Epidemiology of cardiac arresi and resuscitation in children. Ann Emerg Med. 1983; 1 2:672-674.
2. Zaritsky A. Selected topics of conrroversies in pediatric cardiopulmonary resuscitation. Crit Care CUn. 1988;4:735-750.
3. O'Rourke PP. Outcome of children who are apneic and pulseless in the emergency room. Crii Care Med. 1986;14:466-468.
4. American Heart Association-, Chameides L, ed. Textbook of Pediatric Advanced Life Support. Dallas, TX: American Heart Assoication; 1988.
5. Seidel JS, Henderson DP, eds. Prehospital Care of Pediatric Emergencies. Los Angeles, CA: Los Angeles Pediatric Society; 1987.
6. Perlcin RM, Levin DL. Shock in the pediatric patient. Part I. ; Pediatr. 1982:101:163169.
7. Schwaitzberg SD, Bergman KS, Harris BH. A pediatric trauma model of continuous hemorrhage. J Pediatr Surg. 1988:23:605-609.
8. Kanter RT, Zimmerman JJ, Strauss RN. Pediatric emergency intravenous access: evaluation of a protocol. Am ) Dis Child. 1986.140:132-134.
9. Perkin RM, Levin DL. Shock in the pediatric patient. Part II. Therapy. J Pediatr. 1982:101:319-332.