Chest Compression, Medications, and Special Problems in Neonatal Resuscitation



Chest Compression, Medications, and Special Problems in Neonatal Resuscitation


Myra Wyckoff and Jay P. Goldsmith



Importance of Effective Ventilation


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.31 When effective ventilation is the primary focus of a newborn resuscitation team, chest compressions and medications are rarely needed in the delivery room. Data from a busy inter-city delivery service with a highly trained resuscitation team suggests that chest compressions are provided for 0.1% of all deliveries51 and chest compressions plus medications in 0.06%.3 Premature newborns have higher rates of receiving chest compressions than their term counterparts.33,60,82 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 despite 30 seconds of what would otherwise appear to be effective ventilation. Specific steps to improve ventilation before starting chest compressions are provided with the mnemonic algorithm MRSOPA (Table 35-1), which includes checking for a good mask seal, repositioning the infant in the open airway position, suctioning the oropharynx for possible obstructing secretions, opening the mouth so that ventilation attempts are not just through the higher resistance nasal passages, increasing the peak inspiratory pressure of the PPV device, and placing an advanced airway such as a laryngeal mask airway or endotracheal intubation.31,33 Thus, if at all possible, the airway should be secured and ventilation provided via the 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, and use of an end-tidal CO2 (ETCO2) detector. A neonatal pig study of asphyxia-induced asystole found that although there was no difference in success of achieving return of spontaneous circulation when the initial steps of resuscitation (dry, position, suction if needed, and stimulation) were followed by 60 seconds of ventilation before compressions, when initial steps were followed by 90 seconds of ventilation before supporting the circulation with compressions, rates of return of spontaneous circulation were decreased.65 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.



Current resuscitation guidelines recommend that initial PPV be provided with 21% O2 and oxygen supplementation guided by pulse oximetry and oxygen saturation per minute-of-life norms; however, once chest compressions are initiated, it is recommended that 100% O2 be used until the heart rate is stabilized.31 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% O2 is avoided.36,73 Some studies suggest that 100% O2 and 21% O2 are equivalent,50,64 and others suggest that more rapid re-establishment of adequate cerebral circulation is obtained when 100% O2 is used.53,63 Two clinical reports suggest that following asphyxia and resuscitation, newborns who demonstrate early hyperoxia in the NICU have worse neurologic outcomes.30,59 There are no randomized studies to determine whether the 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 seems to be to resuscitate with supplemental oxygen when chest compressions are necessary, with weaning as soon as possible once the heart rate is stabilized to limit exposure to hyperoxia.



Chest Compressions


Chest compressions should be centered over the lower one third of the sternum to compress most directly over the heart.21,29,49,52 Compressing 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, blood enters the heart from the veins.31 Chest radiographs of 55 infants between 27 weeks’ gestation and 13 months’ post-term demonstrate that the center of the heart is positioned under the lower third of the sternum in 87% of cases with 7% slightly more cephalad, but still below the lower half of the sternum.52 For 6% of infants, the position is below the xiphisternal junction. Another study of 55 children between the ages of 1 day to 19 years, including eight premature infants, verified via chest films or right-sided heart angiography, that the center of the cardiac silhouette and/or right ventricle lay under the lower third of the sternum in all age groups.21 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.49 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.49 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.12 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 in almost all circumstances of neonatal chest compressions (Figure 35-1, A). The less effective two-finger method uses the tips of the middle and index fingers to depress the sternum while the other hand provides a firm surface behind the newborn’s back (see Figure 35-1, B). Evidence from animal models of asphyxia-induced asystole demonstrate that the two-thumb technique generates higher blood pressures than the two-finger technique.26 This has also been shown in a manikin model with a customized artificial arterial system.18 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.11,27 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.14,69 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. Resuscitators with small hands have preferred the two-finger technique when they cannot get their hands around the torso of a large baby. 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.


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Figure 35-1 A, Correct thumb technique of chest compression. B, Correct finger position for chest compression. (Adapted from Kattwinkel J, eds. Textbook of neonatal resuscitation. 5th ed. Copyright American Heart Association/American Academy of Pediatrics; 2006.)

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 of the chest has been used to determine the chest dimensions of neonates and young infants.7,46 These studies 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.44 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 the primary goal of chest compressions is to perfuse the heart and brain while awaiting definitive restoration of a cardiac rhythm. 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.29 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.16,29 The chest must be allowed to fully recoil before the next compression so that the heart can refill with blood.


The ratio of compressions to ventilations that would truly optimize perfusion and ventilation during resuscitation from asphyxial arrest is unknown.78 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,4,5 especially during prolonged resuscitation.17 Physiologic mathematical modeling suggests that higher compression-to-ventilation ratios would result in underventilation of asphyxiated infants.2,78 Such models predict that three to five compressions to one ventilation should be most efficient for newborns. The current Neonatal Resuscitation Program guidelines recommend a ratio of three compressions to one ventilation breath such that 90 compressions and 30 breaths per minute are achieved. The two 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.”31 Recent studies have compared 3 : 1 to 9 : 3 compression to ventilation ratios65 and 3 : 1 to 15 : 2 ratios66 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 two-minute interval.24 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. Concern that compressions delivered at the same time as a ventilation breath might impede effective ventilation, have 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. Asynchronous and simultaneous delivery of compressions and ventilations has not been studied in newborns or appropriate models of asphyxia-induced arrest. In adult cardiac arrest (ventricular fibrillation) models, simultaneous delivery confers no advantage.6,25


Strategies for optimizing the quality of the compressions and ventilations with as few interruptions as possible should be considered. The most recent NRP recommendations (2011) lengthened the interval between auscultation pauses to at least 1 minute in an effort to decrease interruptions in perfusion.31 It is possible that quantitative ETCO2 monitoring can serve as a noninvasive tool to eliminate frequent auscultation pauses during CPR. Changes in ETCO2 primarily reflect changes in cardiac output during CPR.85 A piglet model of asphyxia-induced asystole demonstrated that once effective PPV is provided, ETCO2 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. Return of spontaneous circulation correlates with a sudden rise in ETCO2 as the re-established perfusion brings CO2 laden blood back to the lungs. An ETCO2 greater than 15 mm Hg correlates well with return of an audible heart rate greater than 60 beats per minute in the newborn pig model.9 Clinical correlate studies are currently underway.



Medications


Epinephrine


When asphyxia is severe enough to result in asystole or agonal bradycardia despite provision of well-coordinated chest compressions and ventilations, the newborn heart is depleted of energy substrate (ATP) and can no longer beat effectively.78,79 Oxygenated blood must be restored to the coronary circulation, or return of spontaneous circulation 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;35 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, steps to improve ventilation followed by coordinated chest compressions and ventilation, then 0.1 to 0.3 mL/kg of 1 : 10,000 epinephrine solution should be given rapidly via the intravenous route followed by 0.5 to 1.0 mL of normal saline flush.31 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.84 The endotracheal route is no longer considered efficacious or reliable for epinephrine delivery.83 Newborn transitional physiology limits the success of the endotracheal route because the decreased pulmonary blood flow may be insufficient to transport drugs from the alveoli to the central circulation, pulmonary vasoconstriction from acidosis could impede drug absorption, unresorbed alveolar fluid may dilute the epinephrine, and potential right-to-left intracardiac shunts could bypass the pulmonary circulation altogether.78 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 : 10,000 epinephrine should be used in hopes of improving efficacy.32 Loading endotracheal epinephrine doses in a larger 3- to 5-mL syringe to alert the resuscitation team as to 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.19 A recent neonatal simulation study found that health care providers could quickly obtain the intraosseous route for delivery of epinephrine.56 No other vasoconstrictor agents for neonatal CPR have been reported.



Volume


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. Most infants who have undergone intrauterine asphyxia and delivery room CPR are not hypovolemic.80 In some circumstances, however, hypovolemic shock is a real possibility (Box 35-1). Shock at birth may be caused by asphyxia, hypovolemia, or sepsis. In addition, most causes of hypovolemic and septic shock result in neonatal asphyxia. Most severely hypovolemic and septic infants are asphyxiated, but 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.42,86 The difficulty is in distinguishing hypovolemic and septic shock from asphyxial shock that does not involve hypovolemia.



Box 35-1   Causes of Hypovolemia




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.76 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, volume expansion should be considered.


In an acute situation, the volume expander of choice is normal saline or lactated Ringer’s solution; although 5% albumin was used in the past, it has no advantage over crystalloid solutions and some evidence of increased risk for subsequent pulmonary edema and thus is not included in neonatal resuscitation guidelines.48 The best volume expander, although rarely immediately available, is whole O-negative blood; this provides volume, oxygen-carrying capacity, and colloid. In an emergency situation, blood can be withdrawn from the fetal side of the placenta and infused into the infant. Although this should very rarely be necessary, if it must be done, it should be performed in a sterile manner as soon as possible after the placenta is delivered. The syringe used to withdraw the blood should be heparinized, and a filter should be attached to the syringe so that microclots can be filtered out before entering the syringe. Before the blood is infused into the infant, the filter should be changed, and blood should be passed through the filter a second time during the infusion. Infusion of volume expanders should consist of a volume of 10 mL/kg given over 5 to 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.




Intravenous Access


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 to 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. 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 35-2 presents an overview of the medications used in delivery room resuscitation, including concentration, dosage, route, and precautions.


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Jun 6, 2017 | Posted by in PEDIATRICS | Comments Off on Chest Compression, Medications, and Special Problems in Neonatal Resuscitation

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