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Advanced resuscitation in the delivery room is rarely needed as long as effective ventilation is quickly established. When compressions are needed, it is critical to minimize pauses, use the most effective two-thumb method from the head of the bed position, and coordinate with breaths that inflate the lung. In rare cases of profound asphyxia, intravenous epinephrine may be needed to reestablish adequate coronary perfusion pressure. Medical personnel who attend deliveries should practice these rare but vital steps so that when a crisis delivery occurs, they can mobilize additional help rapidly and perform the needed steps with skill without hesitation.
Accurate recording of the events in the delivery room and deliberate team debriefing should be employed to drive constant improvement in management of complex resuscitations.
Effective positive pressure ventilation (PPV) is the most critical action needed to stabilize a newborn infant that is compromised at delivery. This is because the most likely cause of cardiovascular collapse of a newborn is asphyxia (inadequate gas exchange). When effective ventilation is the primary focus of a newborn resuscitation team, chest compressions and medications are rarely needed. Data from a busy intercity delivery service with a highly trained resuscitation team suggests that chest compressions are provided for 0.1% of all deliveries and chest compressions plus medications in 0.05%. Premature newborns have higher rates of receiving chest compressions than their term counterparts.
The most recent Neonatal Resuscitation Program (NRP) guidelines from the American Heart Association and the American Academy of Pediatrics suggest that chest compressions be performed if the heart rate remains less than 60 beats per minute after ventilation that inflates the lungs, as evidenced by chest rise with ventilation breaths. Specific steps to improve ventilation before starting chest compressions should be initiated using the mnemonic algorithm MRSOPA ( Table 34.1 ), which includes checking for a good m ask seal, r epositioning the infant in the open airway position, s uctioning the oropharynx for possible obstructing secretions, o pening the mouth so that ventilation attempts are not just through the higher resistance nasal passages, increasing the peak inspiratory p ressure of the PPV device, and placing an advanced a irway such as a laryngeal mask airway or endotracheal intubation. Thus, if at all possible, the airway should be secured and ventilation provided via an advanced airway before initiation of chest compressions. The increased focus on achieving effective ventilation means that some extra time is allowed to work on the MRSOPA steps before proceeding to chest compressions. Common sense must prevail in the uncommon circumstance when neither a laryngeal mask airway nor endotracheal tube can be placed successfully. In this situation, chest compressions may have to be started while continuing to focus on optimization of mask ventilation. This can be accomplished by observation of adequate chest rise, bilateral auscultation of the lungs, and use of an end-tidal CO 2 (ETCO 2 ) detector. A neonatal pig study of asphyxia-induced asystole found no difference in rates of return of spontaneous circulation when the initial steps of resuscitation (dry, position, suction if needed, and stimulation) were followed by 30 versus 60 seconds of ventilation before compressions were started; however, 90 seconds of ventilation before supporting the circulation with compressions decreased rates of return of spontaneous circulation. There is no evidence regarding optimal length of ventilation before compressions in the situation of severe bradycardia rather than asystole. There is no clinical evidence to offer guidance in either circumstance.
M | Mask | Check mask seal |
R | Reposition | Position in open airway “sniffing” position |
S | Suction | Suction to remove obstructing secretions |
O | Open the mouth | Open the mouth to decrease resistance |
P | Pressure increase | Increase the peak inspiratory pressure |
A | Advanced airway | Place a laryngeal mask airway or intubate |
Current resuscitation guidelines recommend that initial PPV be provided with 21%-30% oxygen in preterm infants <35 weeks of gestation and with 21% oxygen in the remaining older preterm and term infants. Oxygen supplementation should be guided by pulse oximetry and oxygen saturation per minute-of-life norms; however, when chest compressions are initiated, it is recommended that 100% O 2 be used until the heart rate is stabilized. This recommendation remains controversial, and clinical data for guidance are lacking. Animal studies of profound cardiovascular collapse caused by asphyxia provide mixed results, with some suggesting a protective effect when 100% O 2 is avoided. Other studies suggest that 100% O 2 and 21% O 2 are equivalent, and still others suggest benefits when 100% O 2 is used. Two clinical reports suggest that following asphyxia and resuscitation, newborns who demonstrate early hyperoxia in the neonatal intensive care unit (NICU) have worse neurologic outcomes. There are no randomized studies to determine whether hyperoxia is causal for neurologic injury or merely a marker of a more severe asphyxial insult that needed more oxygen for stabilization. The best compromise for the clinician at the present time continues to be to resuscitate with supplemental oxygen when chest compressions are necessary (as ventilation with room air will have already been tried by this point), with weaning of the oxygen as soon as possible once the heart rate is stabilized to limit exposure to hyperoxia.
The most common reason for why a newborn fails to successfully transition at birth is lack of gas exchange resulting in simultaneous hypoxia and mixed metabolic and respiratory acidosis, otherwise known as asphyxia. Combined profound hypoxia and acidosis depresses myocardial function and promotes maximal vasodilation. The goal of chest compressions is to mechanically pump the blood through the heart until the myocardium is sufficiently oxygenated to recover spontaneous function. Due to preferential perfusion of the heart and brain during cardiac compressions, greater than 50% of normal cardiac and cerebral blood flow can be achieved through optimized cardiac compressions. Improved myocardial perfusion increases the likelihood of faster return of spontaneous circulation, while improved cerebral perfusion positively impacts neurologic outcome.
Chest compressions should be centered over the lower one-third of the sternum to compress most directly over the heart. Compression of the sternum directly over the heart squeezes it against the spine. This increases intrathoracic pressure, which causes blood to be pumped from the heart into the arteries. When the pressure on the sternum is released, venous blood refills the heart and blood flows into the coronary arteries. Chest radiograph studies demonstrate that the center of the infant heart is positioned under the lower third of the sternum the majority of the time. Ten pediatric patients (between 1 month and 3 years of age) who sustained cardiac arrest and had arterial pressure monitoring lines in place were monitored during external chest compressions performed by medical providers who were blinded to the blood pressure monitoring. Compressions were provided in random order either at the level of the patient's nipples (midsternum) or over the lower one-third of the sternum above the xiphoid. Each patient served as his or her own control with compressions performed at both locations in random sequence. The performance of compressions over the lower one-third of the sternum resulted in significantly better systolic and mean arterial blood pressures. A more recent study of 63 infants confirmed that location of the left ventricle in 90% of cases was under the lower 1/3 of the sternum using infant CT scan measurements. Although there is one report of CT scan measurements for 75 infants with a mean age of 4.4 ± 3.6 months, which found the heart to be located under the lower 1/4 of the sternum, care must be taken to not be too low on the sternum to avoid dislocation of the xiphoid process, which could lead to liver laceration. Similarly, placement of the compressing thumbs must be centered over the sternal bone so as to not cause rib fractures, which could inhibit critical ventilation via pneumothoraces or a flail chest.
The two-thumb technique in which the hands encircle the chest while the thumbs compress the sternum should be used for neonatal chest compressions. The older, less effective two-finger method is no longer recommended. Evidence from animal models of asphyxia-induced asystole demonstrate that the two-thumb technique generates higher blood pressures than the two-finger technique. This has also been shown in a manikin model with a customized artificial arterial system. Manikin studies demonstrate that the two-thumb technique improves depth of compression, lessens fatigue of the compressor, and results in more consistently accurate thumb placement on the sternum than the two-finger technique. Clinical data are limited to a few case reports but also suggest that the two-thumb technique generates better perfusion pressures than the two-finger technique in newborns. In the past, the two-finger technique was used primarily as a means of keeping the compressor's arms out of the way while emergent umbilical venous line placement was obtained. With the implementation of the MRSOPA algorithm and securing an advanced airway before initiation of compressions, the compressor can move to the head of the bed once the tube or laryngeal mask is secured and continue the more effective two-thumb technique even while emergent intravenous access is obtained. It is crucial that compressions from the head of the bed never interfere with adequate ventilation and establishment of an advanced airway.
Optimal compression depth for the newborn is believed to be one-third the anterior-posterior (AP) diameter of the chest and thus varies with the size of the baby. Computed tomography images of the chest of neonates and young infants estimate that a compression depth of half the AP diameter might result in internal organ damage but that one-third the AP diameter would lessen this risk while still resulting in enough compression of the heart to generate blood flow. Clinical data are limited to a report of six infants who had arterial lines in place after cardiac surgery and subsequent cardiac arrest. Chest compressions were given to a depth of one-third the AP diameter and subsequently one-half the AP diameter. Although a compression depth of one-half the AP diameter resulted in higher mean arterial pressures, this was mainly owing to an effect on systolic blood pressure. Diastolic pressures between the two groups were similar. This is an important distinction, because coronary perfusion pressure is determined by aortic diastolic blood pressure minus the right atrial diastolic blood pressure, so it is the diastolic blood pressure that is most critical. It has also been noted that a compression-to-relaxation ratio with a slightly shorter compression than relaxation phase offers theoretical advantages for blood flow in the very young infant. The chest must be allowed to fully recoil before the next compression so that the heart can refill with blood.
The best ratio of compressions to ventilations to optimize perfusion and ventilation during neonatal resuscitation is unknown. It is clear from animal models that ventilations in combination with chest compressions result in better outcomes than if resuscitation proceeds with ventilations or compressions alone, especially during prolonged resuscitation. Physiologic mathematical modeling suggests that higher compression-to-ventilation ratios would result in underventilation of asphyxiated infants. Such models predict that three to five compressions to one ventilation should be most efficient for newborns. The current NRP guidelines recommend a ratio of three compressions to one ventilation breath such that 90 compressions and 30 breaths per minute are achieved. The medical providers performing the compressions and ventilations should communicate by having the compressor count the cadence out loud as “one and two and three and breathe and.” Studies have compared 3 : 1 to 9 : 3 compression-to-ventilation ratios and 3 : 1 to 15 : 2 ratios in newborn pig models of asystole caused by asphyxia. Although the 15 : 2 ratio provided more compressions per minute without compromising ventilation as measured by arterial blood gas and generated statistically higher diastolic blood pressures, the diastolic blood pressure was still inadequate until epinephrine was given, and thus there was no difference in the time to stabilize the heart rate. A manikin study of 3 : 1, 5 : 1, and 15 : 2 compression-to-ventilation ratios using the two-thumb technique compared depth of compressions, decay of compression depth over time, compression rates, and breaths delivered over a 2-minute interval. Providers using the 3 : 1 versus 15 : 2 ratio achieved a greater depth of compressions as well as more consistent depth over time. The 3 : 1 ratio delivered the most breaths and fewest compressions, as would be expected. Thus, there is no evidence from human, animal, manikin, or mathematical modeling studies to warrant a change from the current compression-to-ventilation ratio of 3 : 1. Rescuers may consider using higher ratios (15 : 2) if the arrest is believed to be of cardiac origin.
Concern that simultaneous compressions and ventilation breaths might impede effective ventilation has led to continued emphasis that compressions and ventilations should be coordinated during neonatal cardiopulmonary resuscitation (CPR), so that they do not interfere with each other. Although studies of asynchronous chest compressions and ventilation (CCaV) show improved minute ventilation, there was no improvement in return of spontaneous circulation (ROSC). CCaV is associated with increased rescuer fatigue and poor quality chest compressions as well as increased left ventricular lactate levels, possibly from trauma or anaerobic metabolism. Recently, neonatal animal model studies and a randomized feasibility study in a small number of neonates showed shorter time to ROSC with continuous chest compressions during sustained inflation. A larger clinical trial is underway to determine if continuous chest compressions during a sustained inflation results in increased ROSC in neonates receiving CPR.
Strategies for optimizing the quality of the compressions and ventilations with as few interruptions as possible should be considered. NRP currently recommends that the interval between auscultation pauses be at least 1 minute in an effort to decrease interruptions in perfusion. Once compressions are initiated, cardiac monitoring leads should be placed so that pauses for auscultation of heart rate can be minimized. It can take a team 17 seconds to complete the auscultation process during delivery room resuscitation when using a stethoscope. When the cardiac monitor heart rate is greater than 60 beats per minute, it is important to confirm by auscultation that the displayed heart rate is not just pulseless electrical activity.
Quantitative ETCO 2 monitoring can serve as a noninvasive tool to eliminate frequent auscultation pauses during CPR. Changes in ETCO 2 primarily reflect changes in cardiac output during CPR. A piglet model of asphyxia-induced asystole demonstrated that once effective PPV is provided, ETCO 2 plummets to near zero with loss of pulmonary blood flow and then increases slightly with initiation of chest compressions, reflecting some blood being pumped through the lungs by the chest compressions. ROSC correlates with a sudden rise in ETCO 2 as the re-established perfusion brings CO 2 -laden blood back to the lungs. An ETCO 2 greater than 15 mm Hg correlates well with return of an audible heart rate greater than 60 beats per minute in a newborn pig model. A single case report of CPR in a very preterm infant at birth noted ROSC just after ETCO 2 reached 12 mm Hg during the resuscitation. Clinical correlate studies are currently underway.
When asphyxia is severe enough to cause asystole or agonal bradycardia despite initiation of CPR, the newborn heart is depleted of energy substrate (adenosine triphosphate [ATP]) and can no longer beat effectively. Oxygenated blood must be restored to the coronary circulation, or ROSC with a heart rate greater than 60 beats per minute will not be achieved. During CPR, coronary blood flow occurs exclusively during diastole, presumably because of increased intramyocardial resistance and increased right atrial pressure during chest compressions ; therefore, coronary perfusion pressure is determined by the aortic diastolic blood pressure minus the right atrial diastolic blood pressure. Given the profound acidemia and resultant vasodilation induced by severe asphyxia, a vasoconstricting pressor agent such as epinephrine is frequently required to attain sufficient aortic diastolic pressure to improve coronary perfusion during newborn CPR. Consequently, if the heart rate remains less than 60 beats per minute despite 30 seconds of effective positive pressure ventilation (with chest rise), followed by coordinated chest compressions and ventilation, then 0.1-0.3 mL/kg of 1 mg/10 mL epinephrine solution should be given rapidly via the intravenous (IV) route followed by 0.5-1.0 mL of normal saline flush.
Data regarding optimal dosing for intravenous epinephrine during newborn CPR are lacking. Intravenous rather than endotracheal delivery of epinephrine is preferred and mandates that delivery room resuscitation providers be well trained in rapid preparation and placement of umbilical venous catheters. In a newborn lamb model of asphyxia, endotracheal (ET) epinephrine was absorbed slowly compared to IV epinephrine, which resulted in lower plasma concentration and less effectiveness. In addition, the absorption of ET epinephrine was delayed, which increases chances of very high epinephrine levels after multiple doses of ET epinephrine in animals who achieved ROSC. Similarly, a recent retrospective cohort study in newborns who required CPR in the delivery room also noted that only 20% of newborns responded to ETT epinephrine alone even though the recommended ET dose was increased compared to a decade earlier. The total dose of epinephrine delivered was higher when any ET epinephrine was given. This might increase risk of arrhythmia or other adverse outcomes due to higher plasma epinephrine levels.
Newborn transitional physiology limits the success of the endotracheal route, because the decreased pulmonary blood flow may be insufficient to transport the drug from the alveoli to the central circulation, pulmonary vasoconstriction from acidosis may impede drug absorption, unresorbed alveolar fluid may dilute the epinephrine, and potential right-to-left intracardiac shunts could bypass the pulmonary circulation altogether. Based on current evidence, once the airway is secured and CPR initiated, immediate attention should be on establishing IV access so that IV epinephrine can be given. The endotracheal route should be used only until IV access is available. However, if the endotracheal route must be tried because of inability to obtain intravenous access, a higher dose (0.5-1.0 mL/kg) of 1 mg/10 mL epinephrine solution may be used in hopes of improving efficacy. Loading endotracheal epinephrine doses in a larger 3- to 5-mL syringe to alert the resuscitation team as for which route the dose is intended can help avoid accidentally giving the higher endotracheal dose through the umbilical line. Successful resuscitation of newborns using the intraosseous route for epinephrine delivery has been reported. A neonatal simulation study found that health care providers could quickly obtain the intraosseous route for delivery of epinephrine. Neonatal resuscitation teams should routinely practice emergent placement of whatever kind of line is used most often at their institution.
At this time, the only other vasopressor that has been studied for use during neonatal CPR is vasopressin. In a newborn piglet asphyxia model, vasopressin improved survival and resulted in lower postresuscitation troponin levels and less hemodynamic compromise compared to epinephrine. This epinephrine alternative needs to be evaluated further before any recommendation can be made.
Although an asphyxiated infant may be in shock, this is not usually caused by hypovolemia but rather by decreased myocardial function and decreased cardiac output from asphyxia. Most infants who have undergone intrauterine asphyxia and delivery room CPR are not hypovolemic. In some circumstances, however, hypovolemic shock is a real possibility ( Box 34.1 ). Shock at birth may be caused by asphyxia, hypovolemia, or sepsis. In addition, most causes of hypovolemic and septic shock result in neonatal asphyxia. Although most severely hypovolemic and septic infants are asphyxiated, most septic or asphyxiated infants are not hypovolemic. Some studies have shown that antepartum asphyxia is associated with increased transfer of blood from the placenta to the fetus before birth, resulting in normal or increased circulating blood volume. The difficulty is in distinguishing hypovolemic and septic shock from asphyxial shock that does not involve hypovolemia.
Decreased blood return from placenta
Cord compression resulting in venous, but not arterial, occlusion
Placental separation compromising placental blood return to the fetus
Hemorrhage from the fetal side of the placenta
Fetal-maternal hemorrhage
Fetal-fetal transfusion
Incision of the placenta during cesarean delivery
Velamentous insertion of umbilical cord with fetal arterial rupture
A history of bright red vaginal bleeding just before delivery, a cesarean delivery where the uterine incision had to be made through an anterior placenta, or the finding of a velamentous insertion of the umbilical cord can raise suspicion for acute fetal blood loss. Placental abruption is a major cause of asphyxia but rarely is associated with fetal blood loss unless caused by trauma such as a high-speed motor vehicle accident. The painful bleeding of abruption is almost always maternal blood loss. Maternal fever, fetal tachycardia, and other signs of chorioamnionitis may indicate neonatal sepsis and shock. Volume expanders may be detrimental in an infant who is not hypovolemic, especially one who has experienced hypoxia-induced myocardial dysfunction. Volume expanders should be given in the acute circumstance when, after adequate ventilation and oxygenation have been established, poor capillary filling persists, and there is evidence or suspicion of blood loss with signs of hypovolemia. In an infant in whom the pulse cannot be normalized despite adequate resuscitation, measures including epinephrine and volume expansion should be considered.
In an acute situation, the volume expander of choice is normal saline; although 5% albumin was used in the past, it has no advantage over crystalloid solutions, and there is some evidence of increased risk for subsequent pulmonary edema and, thus, it is no longer included in neonatal resuscitation guidelines. Lactated Ringer's has never been studied in neonatal resuscitation and for simplification of stocking delivery room neonatal resuscitation supplies has been removed from the NRP recommendations. The best volume expander, although rarely immediately available, is whole O-negative blood; this provides volume, oxygen-carrying capacity, and colloid. Infusion of volume expanders should consist of a volume of 10 mL/kg given over 5-10 minutes. In true acute hypovolemia, it is often necessary to repeat this infusion a second or third time. In acute hypovolemia, hematocrit may be misleading since not enough time has passed for equilibration to occur. Therefore, with a history of acute blood loss (i.e., ruptured velamentous cord insertion), volume should be given even in the face of a normal early hematocrit.
Other drugs such as sodium bicarbonate, naloxone, and pressor agents other than epinephrine are no longer considered resuscitation drugs for the delivery room. They are discussed briefly in the section Immediate Care after Establishing Adequate Ventilation and Circulation .
Medications should preferentially be given through an umbilical venous catheter. When an umbilical catheter is used, it should be inserted into the umbilical vein just beneath the skin, approximately 2-4 cm until free flow of blood is obtained when the stopcock is opened to the syringe and the syringe gently aspirated. If the catheter is inserted too high and becomes wedged in the liver, solutions can be infused into the liver, which may cause liver necrosis. The depth of insertion of the catheter is much less in premature infants depending on their weight, and care should be taken not to insert the catheter too far. If a catheter is not prepared and ready, endotracheal administration of epinephrine may occur through the endotracheal tube while the catheter is being prepared, but only as a temporizing measure while IV access is established. It is prudent, however, that when preparing for a “crash” delivery, the catheter should be prepared in advance to minimize the delay in giving epinephrine by the most effective route. Table 34.2 presents an overview of the medications used in delivery room resuscitation, including concentration, dosage, route, and precautions.
Medication to Administer | Concentration | Syringe for Preparation | Dosage; Route | Weight of Newborn (kg) | Total Dose (mL) | Precautions |
---|---|---|---|---|---|---|
Epinephrine | 1 mg/10 mL | 1 mL | 0.1-0.3 mL/kg; IV | 1 | 0.1-0.3 | Preferred route; give rapidly |
2 | 0.2-0.6 | |||||
3 | 0.3-0.9 | |||||
4 | 0.4-1.2 | |||||
3 or 5 mL | 0.5-1.0 mL/kg; ET | 1 | 0.5-1 | 5-10 times IV dose; give directly into the ET tube | ||
2 | 1-2 | |||||
3 | 1.5-3 | |||||
4 | 2-4 | |||||
Volume expanders | Normal saline, whole blood | 30 mL | 10 mL/kg; IV | 1 | 10 | Give over 5-10 min |
2 | 20 | |||||
3 | 30 | |||||
4 | 40 |
If an infant still has no heart rate after 10 minutes of what otherwise appears to be effective resuscitation, resuscitation providers may consider discontinuing their efforts. This does not mean that the resuscitation team must stop at 10 minutes after birth, but rather that after 10 minutes of well-coordinated resuscitation efforts if the newborn is still asystolic, it is appropriate to consider discontinuation. The majority of available data indicate that after 10 minutes of asystole, there are few survivors and those who do survive frequently have severe disability. Infants with 10-minute Apgar scores of zero but who survived to be admitted to the NICU and entered into a hypothermia clinical trial had better outcomes than those reported in the systematic review by Harrington; however, there was significant selection bias. Recent cohort studies of infants with 10-minute Apgar scores of zero who were subsequently treated with hypothermia had ~20%-30% survival with normal development on early assessments. Decisions regarding whether to continue or discontinue resuscitative efforts must be individualized. Variables to be considered may include whether the resuscitation was considered optimal; the availability of advanced neonatal care such as therapeutic hypothermia; the specific circumstances before delivery (e.g., known timing of the insult); and the wishes expressed by the family.
A critical member of the neonatal resuscitation team is the recorder, who should document in real time the steps of resuscitation that the team makes and the infant's response. It is not acceptable to write a summary from memory after the fact when the accuracy of the details may be lost. The resuscitation record should be used to debrief the team after every advanced resuscitation to look for opportunities to improve in communication, documentation, resuscitation skills, and knowledge of the algorithm. Some institutions choose to video record delivery room resuscitations for this purpose.
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