Paediatric Resuscitation
Sunita Goel
Lecturer in Anaesthesiology, BJ Wadia Childrens hospital, Mumbai, India
First Created: 01/25/2001 


Survival and neurologic outcome in pediatric cardiac arrest has not improved significantly in the past decade. The prognosis of cardiac arrest in children remains poor with 3 to 17% surviving to hospital discharge; few of the survivors have a good neurological outcome. However, recent developments hold promise for improving the outcome in such patients.


Pediatric resuscitation differs from those of an adult. However, data supporting these differences are lacking particularly because cardiac arrests are rare in children. Therefore, small sample size, inadequate power, lack of standardized terminology, and the retrospective nature of the studies has made a comparison of outcome measures difficult. The paucity of resuscitation outcome data in the pediatric population makes the scientific justification of recommendations difficult. Hence, the optimal method of pediatric resuscitation is still unclear.

In 1995, a pediatric task force developed the Paediatric Upstein Style to provide uniform definitions, time intervals, intervention, and outcomes in a template form. This hopefully, allows for the meta-analysis of smaller studies and encourages larger randomized, multicentre, multinational clinical trials to validate the pediatric resuscitation protocol. The pediatric guidelines include respiratory and cardiac arrest because effective management of respiratory distress prevents progression to cardiac arrest. The terminologies that are derived from the guidelines for uniform pediatric advance life support are:

Cardiac arrest refers to the clinical state characterized by the absence of detectable cardiac activity.

Return of spontaneous circulation (ROSC) refers to the return of any spontaneous central palpable pulses regardless of duration. It can be intermittent or sustained. Sustained ROSC is defined as a duration sufficient to permit the transfer of patient either from the site of the arrest to the emergency department or for in house arrest, to the operating room or intensive care unit. It can also be defined as ROSC of more than or equal to 20 minutes.


The primary etiology of most pediatric cardiac arrest is respiratory arrest, which accounts for 56% to 78% of cases. Respiratory arrest alone has a significantly better outcome because hypoxia is not sufficiently prolonged to cause cardiac arrest. The commonest rhythm in a pediatric arrest is bradycardia leading to asystole, occurring between 77% to 95%, and is secondary to prolonged hypoxia. Ventricular tachycardia and fibrillation occur between 4% and 23%. Primary dysrhythmic cardiac arrest should particularly be considered in patients with underlying cardiac disease or history suggestive of myocarditis.

Airway Management

There is a focus on early ventilation and early effective oxygenation in pediatric resuscitation because cardiac arrest is often secondary to respiratory failure. The most common cause of airway obstruction in the unconscious pediatric patient is the tongue. Head tilt chin lift or jaw thrust particularly in suspected cervical spine instability is important to maintain a patent airway. There is a suggestion that blind removal or attempted visualization of an unsuspected foreign body is unlikely to be effective because foreign bodies causing airway obstruction is unlikely to be visible and attempted removal may dislodge it further distally.

Current recommendation is for mouth to mouth and nose ventilation for infants up to 1-year-old. The number of initial attempted resuscitative breath remains debatable ranging between 2 to 5 in the various algorithms, delivered over 1 to 1.5 seconds. The long inspiratory time is recommended to reduce the airway pressure and hopefully reduce gastric insufflation. Insufflation of the stomach may splint the diaphragm, decrease the lung volume, and increase the risk of aspiration. Face mask ventilation with cricoid pressure has reduced gastric gas volume and increased exhaled volume. Ideal ventilation frequency during CPR is unknown. The current recommendation is based on normal ventilatory rates for age, the need for coordination with chest compression, and the practical ability to perform them. The rescuer should pause between breaths to maximize oxygen and minimize carbon dioxide in the delivered breaths.

Infrequent intubation experience of the pediatric population may result in less than optimal airway management of these patients. Effective bag-valve-mask ventilation especially with a self-inflating bag is more important than fumbled and prolonged attempts at intubation at the scene of cardiac arrest. Gauche et al demonstrated no improvement in survival or neurological outcome between pediatric patients who were randomized to be intubated compared to those who received bag-valve-mask ventilation. Also, two rescuers were able to deliver greater tidal volumes than one with a bag-valve-mask device. Recent literature suggests that the laryngeal mask airway (LMA) can be used in resuscitation and the skills for insertion can be easily acquired. The LMA, though, can only be used in patients with no gag reflex and there is still a small risk of aspiration.


The objective of CPR is to provide adequate oxygenation and perfusion to the vital organs until the return of sustained adequate spontaneous circulation. In animal studies, CPR is able to maintain cerebral and myocardial perfusion at only 20% of the pre-arrest values. Hence, optimal cardiac compression technique and timing are important. There is documented difficulty in reliably assessing the pulse in the pediatric resuscitation and therefore, resuscitative intervention should not be delayed more than 10 seconds to detect a pulse. Chest compression should be started in all pulseless or profound bradycardia pediatric patients over the lower half of the sternum taking care not to compress the xiphoid and to approximately one third the depth of the chest at a rate of 100 compressions per minute. Three studies have confirmed that the heart lies beneath the lower third of the sternum in all ages and chest compression over the lower third produces better arterial pressures and stroke volume than over the mid sternum with no other organ injuries.

Although the most practical assessment of chest compression is pulse detection, there is a suggestion it may represent the retrograde venous flow. End-tidal CO2 detection represents pulmonary blood flow may be a better assessment of chest compression and is predictive of ROSC. The most efficient blood flow is achieved when the cardiac compression lasts 50% of the cycle to allow sufficient time for chest recoil. Cardiac compression can be done with one hand in children up to 8 years old. However, the size of the victim and the strength of the rescuer may necessitate the use of 2 hands in younger children. In infants, encircling the infant's chest and compressing with overlapping thumbs (Thaler-Strobie manoeuvre) may produce higher mean arterial, pulse pressures, and cardiac output, possibly by a greater increase in intrathoracic pressure. However, in an older child, the encircling hand may not allow full re-expansion of the chest, reducing venous return.

The ideal compression-ventilation ratio is unknown but the current consensus is 3: 1 in newborns and 5: 1 in infants and children. This difference from the adult resuscitation guidelines emphasizes that respiratory problems are the most common etiology in pediatric cardiac arrest and that the physiological respiratory rates in this age group are faster. The interposition of compression and ventilation is recommended to avoid simultaneous compression and ventilation.

There are 2 theories of the mechanism of blood flow during CPR: direct cardiac compression and the "thoracic pump" mechanism. The "thoracic pump" mechanism postulates the global increase in intrathoracic pressure associated with cardiac compression results in forward blood flow. Direct cardiac compression assumes that the blood flow is produced by direct compression of the heart between the sternum and the vertebral bodies. This mechanism may play a greater role in the pediatric population as compared to the adults due to the more compliant chest wall.

Alternative Methods of Artificial Circulation

Active compression-decompression CPR (ACD-CPR) was developed after a report of a man who used a plunger to resuscitate a person. This device, which is attached to the chest wall, increases the intrathoracic pressure during compression to promote forward blood flow. During active decompression, it augments the negative intrathoracic pressure that increases the venous return and myocardial perfusion.

The advantages of ACD-CPR are rescuers can perform alone; it is portable and relatively inexpensive. However, it is associated with an increased incidence of local chest trauma and increased fatigue. Clinical studies on ACD-CPR in adults have been inconclusive, mainly due to inadequate power. Currently, no study has been done to assess the use of ACD-CPR in the pediatric population although increased chest wall compliance and flexibility would make ACD-CPR device of significant value. There is also a need to manufacture several sizes and overcome the 15-17% incidence of the device not adhering to the chest wall.

Interposed abdominal compression CPR (IAC-CPR) or counterpulsation is a CPR technique that involves applying pressure to the abdomen during the decompression phase of chest compression. This method apparently increases venous return and acts like an intra-aortic balloon pump by pushing retrograde aortic blood flow to the brain and heart. A second rescuer applies abdominal pressure manually with two hands during diastole and avoids injury to the liver. Animal studies have been promising and some studies in adults have demonstrated improved cerebral and myocardial blood flow leading to increased ROSC and survival to hospital discharge. However, the optimal method of abdominal compression is still unclear. Again, there have been no pediatric studies and there are still concerns about potential abdominal organ injuries in children. Another limitation of the technique is the need for 3 rescuers.

Abdominal binding and simultaneous compression-ventilation CPR (SCV-CPR) is thought to increase cardiac output by augmenting the thoracic pump mechanism. It was able to generate higher arterial pressures in adults but there was no difference in ROSC or survival.

Other invasive circulation methods involve the use of an intra-aortic balloon pump, extracorporeal membrane oxygenation (ECMO), or cardiopulmonary bypass. These methods require time, sophisticated resources, and technical skills to implement. Open cardiac massage should be reserved for penetrating chest injuries who acutely deteriorate in the hospital. Pediatric blunt trauma patients appear not to benefit from open chest massage.

Vascular Access

Successfully resuscitated patients had vascular access significantly earlier than those not resuscitated. Rapid delivery of drugs into the central circulation combined with effective chest compression is necessary to deliver adrenaline to its site of action in the vascular tree.

The intravenous and intraosseous route is preferred for the delivery of drugs. Central venous drug administration produces a more rapid and higher peak concentration than peripheral venous administration in adults. A fluid bolus improves the delivery of drugs into the central circulation. Injection into veins that drain into the superior vena cava is better than to veins that drain into the inferior vena cava because the inferior vena cava does not effectively collapse resulting in to and fro blood flow.

There is consensus that the tibial intraosseous route is useful for vascular access for patients up to 6 years of age. The peak effects and duration of action of drugs given intraosseous were comparable to central and peripheral venous routes. The small risk associated with the intraosseous routes such as fractures, growth plate injuries, subcutaneous or subperiosteal infusions, compartment syndrome, fat embolism, and osteomyelitis, which occurred only after infusion of hypertonic solution or prolonged infusions. Contraindications to the intraosseous route include osteogenesis imperfecta, osteopetrosis, ipsilateral limb fracture, or local infection.

The endotracheal route may be used if vascular access is delayed. Certain lipid-soluble drugs such as adrenaline, lignocaine, and atropine can be given via the endotracheal tube but the drug absorption kinetics is not favorable. However, drugs such as bicarbonate, glucose, and calcium can cause serious lung injuries. Ten times the amount of drugs given intravascularly needs to be given through the endotracheal tube to achieve the same plasma drug concentration and peak drug action. However, the lung acts as a depot for these large amounts of drugs and the child may have profound and prolong hypertension upon ROSC due to slow absorption of the adrenaline depot. Drug absorption is most efficient at the alveoli and small airway. Therefore, drugs should be delivered via a catheter into the lower airways beyond the tip of the tracheal tube or followed by a 5 ml saline flush and 5 mechanical insufflations to aid distribution. After 15 minutes of CPR, the tracheal route may be less effective due to pulmonary edema and atelectasis.


Adrenaline remains as the only drug that is effective in restoring circulation in cardiac arrest. The consensus initial dose is 0.01 mg/kg intravascularly or 0.1 mg/kg by the endotracheal route. The subsequent doses should be 0.1 mg/kg at a 3 to 5-minute interval to allow the peak effect of intravascular adrenaline to take place. Its mechanism of action is believed to be its a-adrenergic activity that increases the aortic diastolic pressure and hence, myocardial perfusion. Adrenaline also selectively diverts blood flow to the vital organs such as the brain and heart from the skin, muscle, and splanchnic circulation. However, adrenaline increases myocardial oxygen demand and afterload.

Strangely, though, studies using pure a-agonist such as methoxamine and phenylephrine have not demonstrated any clear benefit over adrenaline. This is possibly the beneficial b 1 effect on cerebral vasodilatation. Noradrenaline, which has both a and b 1 effects without b 2 effects, theoretically may be advantageous since it lacks the b 2 smooth muscle vasodilatation which reduces the aortic diastolic pressure. However, it has not been proven to be superior to adrenaline. Recently, vasopressin has been shown to have greater improvement in myocardial and coronary blood flow compared to adrenaline in ventricular fibrillation models. More work needs to be done in this area.

The use of high dose adrenaline in cardiac arrest in adults has not produced optimistic results. Large multicentre trials have demonstrated increased ROSC rates but no improvement in long term survival and neurological outcome. The poor outcome is attributed to the limited improvement in myocardial perfusion in adult patients with coronary heart disease and a fixed cardiac narrowing, from high dose adrenaline is offset by the increase in myocardial demand. There is a suggestion that children with normal coronaries would benefit from high dose adrenaline. However, the benefits of high dose adrenaline in the pediatric population remains unproven due to the small sample size of the studies.

There are concerns over the use of high dose adrenaline. The combination of severe a vasoconstriction with an increase in myocardial oxygen consumption may lead to systemic hypertension, intracranial hemorrhage, ventricular dysrhythmias, myocardial ischemia, and necrosis as it has been shown in some animal studies. There is also the potential that high dose adrenaline may produce more survivors but in a vegetative state.

Poor ventilation and perfusion lead to mixed respiratory and metabolic acidosis during cardiac arrest. It is believed that acidosis reduces the effectiveness of adrenaline, myocardial contractility, increases pulmonary vascular resistance but decreases the systemic vascular resistance, and reduces the synthesis of adenosine triphosphate. However, cellular acidosis is poorly reflected by the arterial blood gas. The key treatment for the acidosis is restoration of tissue perfusion. Administration of sodium bicarbonate would theoretically then overcome this problem by buffering the accumulated metabolic acids. However, unless ventilation and perfusion are adequate to eliminate the formed CO2, the Handerson-Hasselbach equation would not proceed to the right. In fact, the increased CO2 formed may worsen the intracellular acidosis. Furthermore, overzealous bicarbonate administration may produce metabolic alkalosis with a left shift of the oxyhemoglobin dissociation curve and poor tissue oxygen delivery, depressed myocardial function, hypokalemia, hypernatremia, and hyperosmolality. Results from animal studies have been encouraging but again the empiric administration of sodium bicarbonate during a prolonged cardiac arrest has not been proven to improve outcomes in humans. Bicarbonate should not be used routinely in pediatric resuscitation but it may be used to transiently increase the pH so that adrenaline is effective in restoring the circulation.

Hypocalcemia in infants may present with poor contractility because contractility is more dependant on extracellular calcium as the intracellular calcium release from the sarcoplasmic reticulum is deficient. However, recent data suggest that calcium antagonizes the action of adrenaline and its major action on blood pressure is due to vasoconstriction rather than positive inotropic action. Furthermore, there is concern that calcium administration may worsen reperfusion injury. Hence, calcium is only indicated to correct documented ionized hypocalcemia and to antagonize the actions of hyperkalemia, hypermagnesemia, and calcium channel blocker toxicity.

Magnesium is useful in the treatment of tachyarrhythmias especially those resistant to lignocaine, torsades de pointes and preventing arrhythmias post-myocardial infarct. However it's role, dosage, and administration in CPR is uncertain.

Lignocaine has been recommended for the treatment of ventricular tachycardia and ventricular fibrillation based on its extensive use in adults. It is a membrane-stabilizing drug that will cause myocardial depression and may stabilize existing arrhythmias.

Bradycardia in children is often due to hypoxia and should be treated with adequate oxygenation. Atropine can be used to antagonize excessive vagal stimulation with 0.02 mg/kg. A minimum of 0.1 mg should be used based on a study that demonstrated paradoxical bradycardia with lesser doses in infants.

Adenosine has become the drug of choice for supraventricular tachycardia and is safe and effective in children. Verapamil is however not recommended because it has been reported to produce bradycardia, hypotension, and asystole in infants because of their immature autonomic system and the importance of heart rate in maintaining cardiac output.

Cerebral Resuscitation

There have been efforts to improve neurological outcome post-cardiac arrest patients. Attempts to increase post-ischaemic cerebral blood flow with calcium channel blockers have not shown improvement in neurological outcome. However, cerebral cooling in animal studies has consistently improved neurological outcome. The use of a simple portable external head cooling device requires further investigation.

Automatic External Defibrillator

The benefit of an automatic external defibrillator (AED) in adults has been demonstrated. Sedgwick et al showed that 43% of patients defibrillated within 4 minutes survived and 87% of the survivors were neurologically intact. Successful defibrillation is inversely related to the time of the first shock.

Its use in the pediatric population is limited as the conventional wisdom is that ventricular fibrillation is a rare cause of cardiac arrest in the pediatric population.

However, recent studies have shown that ventricular fibrillation account for 20% of pediatric cardiac arrests. The overall survival rate in patients with ventricular fibrillation was better than patients with pulseless electrical activity or asystole.

The limitation in the use of AED in children are the energy dose, the paddle size, and the reliability of these devices in detecting ventricular tachycardia and ventricular fibrillation. The preset voltage in the AED would exceed the recommended voltage in a child. The initial voltage recommended is 2J/kg increasing to a maximum of 4J/kg in a series of 3 shocks. Whether this would be damaging to the myocardium remains unclear. The chest wall of children older than 8 years old or more than 10 kg is probably large enough to accommodate the adult size paddle. The impedance of the adult paddle is approximately half of the children's paddle.


The outcome of cardiac arrest in children is typically poor, reflecting the fact that cardiac arrest does not occur until the child's physiological reserves have been exhausted. Since pediatric cardiac arrest follows a progressive deterioration of cardiorespiratory function, the degree of ischemia, acidosis, and organ dysfunction is greater than in acute arrest from ventricular defibrillation. This may reduce the likelihood of recovery. Certain situations are associated with better resuscitative outcomes

  1. Witnessed arrest - shorter interval between arrest and starting basic life support improves survival
  2. In hospital cardiac arrest - presumably because of more rapid treatment.
  3. Bystander CPR
  4. Emergency medical team arrival within 10 minutes
  5. Resuscitation lasting less than 20 minutes
  6. Fewer than 2 doses of adrenaline
  7. Return of spontaneous circulation before arrival in hospital (exception hypothermic patient)
  8. Ventricular fibrillation - 40% survival as compared with 3% from asystole

Neurologically intact survival is associated to prompt resuscitation and more likely with respiratory rather than cardiac arrest. Furthermore, the sequence of resuscitation actions should consider the most likely cause of the arrest. However, whether this method improves the outcome remains to be studied. There have been efforts to assess the cost-benefit of pediatric resuscitation in the emergency department. As in adults, pediatric patients who fail to respond to prehospital resuscitation are unlikely to respond in the emergency department. There is a reluctance to limit the resuscitation to the pre-hospital setting because pediatric deaths are unexpected and tragic. Furthermore, it is generally thought that children do not receive optimal resuscitation prehospital advanced life support.

The end-tidal CO2 detector has shown promise to differentiate the survivors from the non-survivors. An increase in end-tidal CO2 is often the initial marker for the return of spontaneous circulation. If the end-tidal CO2 was higher than 10 mm Hg at 20 minutes then ROSC did not occur. A disposable semi-quantitative colorimetric end-tidal CO2 detector has been studied in the pediatric population by Bhende and Thompson and has potential prognostic value. Furthermore, it is cheap, portable, and requires no warm-up. The monitor categorizes the end-tidal output into 3 ranges:

  • Less than 0.5%
  • 0.5% to 2.0%
  • 2.0% to 5.0%

Patients who arrived in the operating room with readings less than 0.5% did not have a return of spontaneous circulation. However, patients who had initial readings of 2.0% to 5.0% were positively associated with the return of spontaneous circulation.

There are still no guidelines regarding how long and how aggressive one should resuscitate pediatric cardiac arrest patients although there is move away from protracted efforts, perhaps with the exception of hypothermic patients.


The complication rates from CPR are much lower in children than adults, reported at approximately 3%. Common significant adverse effects are rib fractures, pneumothorax, pneumoperitoneum, retinal hemorrhage, and hemorrhage.

Paediatric Resuscitation Paediatric Resuscitation 01/25/2001
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