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Congenital heart disease causes significant alterations in oxygenation, perfusion, and myocardial function after birth, and it can be categorized into hypoxic and normoxic lesions.
The overall goal of therapy in shock is to treat the underlying cause, return adequate oxygen delivery to the tissues, and remove metabolic products that developed during anaerobic metabolism. It appears that the faster the body returns to adequate perfusion, the better the overall outcome.
One of the specifics for neonatal resuscitation is the recommendation of positive pressure ventilation (PPV) with room air, unless chest compressions or medications are needed during the resuscitation, then the recommendation is still for PPV with 100% oxygen.
Pediatric cardiac arrest is not a rare event. At least 16,000 American children (8-20 per 100,000 children per year) suffer a cardiopulmonary arrest each year.
The four distinct phases of cardiac arrest and cardiopulmonary resuscitation (CPR) interventions are: (1) prearrest, (2) no-flow (untreated cardiac arrest), (3) low-flow (CPR), and (4) post-resuscitation and arrest.
Acute respiratory distress syndrome (ARDS) diagnostic criteria have been revised recently and are now the Berlin Definition, where ARDS is separated into three mutually exclusive categories based on the degree of hypoxia. Mild is PaO <ce:inf>2</ce:inf> /FiO <ce:inf>2</ce:inf> = 201 to 300 with positive end-expiratory pressure (PEEP) > 5, moderate is PaO <ce:inf>2</ce:inf> /FiO <ce:inf>2</ce:inf> = 100 to 200 with PEEP > 5, and severe is PaO <ce:inf>2</ce:inf> /FiO <ce:inf>2</ce:inf> < 100 with PEEP > 10.
Traumatic brain injury (TBI) is composed of two components—an initial primary injury owing to direct mechanical deformation of brain parenchyma and a subsequent secondary injury that can develop over hours to days. Secondary injury may be the result of multiple mechanisms including ischemia, excitotoxicity, metabolic failure and eventual apoptosis, cerebral swelling, axonal injury, and inflammation and regeneration.
A vascular occlusive crisis in the lungs leads to acute chest syndrome (ACS). Acute chest syndrome is the leading cause of death and the second most common complication in sickle cell disease.
Tumor lysis syndrome is a metabolic crisis precipitated by acute lysis of a large number of tumor cells. Serum uric acid, potassium, and phosphate concentrations are elevated. The elevated phosphate concentrations cause hypocalcemia.
The role of family in the pediatric intensive care unit (PICU) has evolved over time, and the inclusion of family in the care of their child is now recognized as an important part of critical care.
Accidents and trauma are the leading causes of death in children 1 to 14 years of age.
Portions of this chapter are taken from Dr. George Gregory’s fine treatment of this topic in the last edition.
The field of pediatric intensive care may have originated from anesthesia, but these areas have grown apart over time. Due to the extensive training, there are few individuals who cover both disciplines. With more complex patients, it is likely that care will occur both in the operating room and the intensive care unit (ICU). There needs to be excellent communication between the ICU and operating room clinicians to ensure a seamless transition of care. Many institutions require an attending to attending handoff between the ICU and anesthesia for each case. It is important that this occurs in the preanesthetic as well as the postanesthetic setting. Information regarding current ICU therapy response can simplify a potentially difficult anesthetic. Similarly, understanding the operative and anesthetic course will guide the next several days of management. A complete anesthesia sign-out includes pertinent past medical history, allergies, ease of mask ventilation, induction agents, ease of intubation, decisions regarding extubation, venous and arterial access, blood products, fluid totals, inotropic agents, medications delivered including timing of antibiotics, complications, laboratory values, and most recent blood gas. This information may be available in the anesthetic record; however, a short verbal summary by the anesthesiologist provides a greater amount of practical detail.
The family is an important part of the critical care team and needs to be included in shared decision making. In pediatric hospitals, families participate in multidisciplinary rounds with their nurses, respiratory therapists, pharmacists, and physician caring for their child. This does not require more time than traditional rounds and it does not compromise teaching. There has been a significant push to increase family participation in both pediatric and adult ICUs. Family engagement is part of the ICU Liberation ABCDEF Bundle that is directed and supported by the Society of Critical Care Medicine. A great amount of information is available at www.iculiberation.org . An international multidisciplinary team of experts in neonatal, pediatric and adult critical care recently published Guidelines for Family Centered Care. The guidelines address the need for family presence in the ICU, the need for family support beyond the ICU; goals for communication, use of consult services such as Palliative Care and Ethics, and a means to address the operational and environmental issues in ICUs that prevent family engagement. We see significant family satisfaction with participation in rounds and we believe it likely benefits the team and patient as well. We anticipate a point in the future where we do not need to prove to anyone the need to have family involvement.
Giving the family a greater presence in the ICU with more responsibility and autonomy in decision making can increase their anxiety and distress. In addition to the potential development of posttraumatic stress disorder (PTSD) in our patients, parents of children admitted to an ICU can incur severe emotional distress. A recent review places the incidence of PTSD in parents of children in the PICU between 10% and 21%, with symptoms of PTSD occurring in up to 84% of families. PTSD can occur no matter how routine the caregivers may view the process. The ICU is a unique and often terrifying experience for families and children. The process of ICU care involves multiple caregivers, changing shifts, and endless physicians. For families in the ICU, there can be a loss of control, significant financial worries, and other factors that affect coping. Helping parents cope with their child’s critical illness and these stressors is a central part of intensive care. Parents may display behaviors that out of context may seem abnormal, such as excessive clinginess, intellectualizing the process, blaming others (including their spouses), minimizing, and seeking opinions everywhere (the internet, environmental care, etc.). We must attempt to understand what drives these behaviors to provide optimal care. We must help the parents be parents and educate them about their child’s illness. This emphasizes that social workers, psychologists, and child and family therapists are all part of the critical care team.
With the move to family-centered care, we must address the issue of parental presence during invasive procedures and cardiopulmonary resuscitation (CPR) efforts. There is increasing literature that families would like to have the choice to stay during CPR events or invasive procedures and the parents do find benefit to being present. We believe that allowing parents to stay during procedures or resuscitation is helpful for the parents coping with the trauma of a critically ill child. As each PICU addresses this issue there are several things to consider. Caregiver attitudes toward parental presence will need to be addressed, as the likelihood of this event increases over time. The decision to allow parental presence cannot be forced on providers. However, we have seen that resistance to family presence among providers is decreasing over time. A means for declining on the part of the clinician as well as the parent must be available. There must be someone identified who will stay with the family and support them. In our ICUs, this role been filled by social workers or members of the clergy. For those who are looking for assistance in making the transition to parental presence during CPR, there have been guidelines published from a national consensus conference. Parental presence during invasive procedures may pose a different challenge as these events occur more frequently compared with CPR. In the same manner, someone other than the person performing the procedure should be looking after the family, even for what we believe to be routine procedures. We also must give younger trainees the opportunity to opt out of family presence during procedures.
A final topic that needs to be addressed is the use of palliative care services for our critically ill patients. There is a role for early consultation of palliative care, as we do not believe in restricting its use or support to just those patients who are near to death. We feel that there is a significant benefit to early engagement for children who are at high risk for mortality during their hospitalization, for children with complex diseases, or those where they cognitive and physical abilities following ICU discharge will be significantly different than previously. There are great benefits to palliative care intervention to provide families ongoing support and opportunities to develop coping mechanisms. Many different PICUs have developed automatic triggers for palliative care consultation, so as not to miss opportunities to improve family support. Examples of triggers can be PICU duration, episodes of CPR, prolonged mechanical ventilation, and specific types of surgeries. A review by the IPAL-ICU (Improving Palliative Care in the ICU) Advisory Board in 2014 addresses the needs and goals of palliative care integration in the PICU.
We believe it is ethically correct to disclosure medical errors to families. However, some clinicians may continue to resist due to concerns regarding litigation. In a survey of 1018 Illinois residents, 27% indicated they would sue, but 38% stated they would recommend the hospital if appropriate disclosure and remediation occurred. The conclusion drawn by the author of the study was that “[p]atients who are confident in their providers’ commitment to disclose medical errors are not more litigious and far more forgiving than patients who have no faith in their providers’ commitment to disclose.” Explanations of medical errors should come from the senior member of the team to the family. This is usually the current ICU attending, but can be the medical director of the ICU, based on the complexity of the incident and outcome. The discussion should include an explanation of what happened in layman’s terms, how it occurred, the repercussions and change of care planned for the child, and what will be done to prevent a similar error in the future. We find it helpful to have the ICU social worker present to help validate concerns and provide support. The attending remains present until all questions are answered or additional time is scheduled if necessary. Most hospitals will track errors or negative outcomes through a quality assurance program. Depending on the incident, a “root cause analysis” should be performed. Medical errors will occur, but they should also be an opportunity to improve practice quality and prevent future events.
In an ICU setting, there unfortunately will also be a need to cope with death and dying. Palliative care plays an important role when nothing medically can be done for the child. We also find their services exceedingly helpful for children with chronic medical conditions who are anticipated to die during a future admission. With a team approach, we try to minimize pain and suffering for the child and family at the end of life. Caregivers in and ICU must understand when to allow the families choices and support them over what may be their own beliefs and practices—as long as the goal remains to prevent further pain and suffering. The awareness of medical futility is increasing over time. However, with this concept there is a significant interplay with financial, societal, ethical, personal, and religious opinions and feelings. It may be difficult to define futility, but when the pain and suffering of continuing life are more severe than the inevitability of death, care may become futile. However, pain relief and caring support for the child and family can never be classified as futile care.
Medical and nursing directors, hospital administrators, and representatives from pediatric medicine, anesthesia, surgery, and the pediatric subspecialties should be responsible for policy and procedures pertaining to the PICU and should make recommendations regarding personnel staffing, equipment purchases, and structural and design changes within the unit. The medical director oversees the quality of patient care, patient triage, implementation of policy and procedures, in-service education, and coordination of consultants. Physician coverage should be full-time geographic at the resident, fellow, and attending staff level, and should include in-house, full-time coverage at night. The nursing director should have special skills in pediatric intensive care, education, and personnel management. The nursing staff must be trained in all aspects of pediatric critical care and resuscitation. Staffing should be flexible enough to provide one-on-one patient care when necessary. A multidisciplinary in-service program is essential for continuing education and orientation. Other team members include respiratory therapists, physical therapists, nutritionists, social workers, laboratory technologists, pharmacists, and psychiatrists and psychologists for the patients and staff. All medical and support personnel should be encouraged to participate in rounds, educational endeavors, and team meetings whenever possible. There must be adequate workspace around each bed and enough storage space to keep life support equipment within reach. Space for reading, meeting, sleeping, and showering should be available for the staff. Space should be provided for parents to remain with their children during the day and for parents to sleep overnight. Parents should be encouraged to participate as much as possible in the care of their child. Each bed space should be standardized so that it can be used to provide any level of care. Private rooms are ideal, but if shared rooms are necessary, the distance between beds must be adequate to ensure privacy and minimize nosocomial infection. Isolation rooms should be available within the confines of the unit. Devices for diversion and entertainment should be available for conscious children. Television and computer games are often better than heavy sedation. Adequate nurses and nursing involvement at the bedside will prevent potentially life-threatening events. Because sick children require close personal observation, centrally monitored nursing stations have little place in the PICU.
The shape of the heart is complete by 6 weeks’ gestation, but myofibrillar density and maturation increase through the first year of postnatal life. During this time, myocytes engage in rapid protein synthesis and rapid cell growth, which requires a high intracellular concentration of nuclei, mitochondria, and endoplasmic reticulum. The greater number of nonelastic and noncontractile elements makes the neonatal myocardium less compliant, and it contracts less efficiently than the adult myocardium. In the fetus and newborn, the decreased ventricular compliance causes small changes in end-diastolic volume to induce large changes in end-diastolic pressure. In addition, augmentation of stroke volume by the Frank-Starling mechanism is less effective in young children. The newborn is more dependent on heart rate (HR) for maintenance of cardiac output. Cardiac output increases only about 15% with volume loading; it increases much more by increasing the HR. This is an important consideration when taking care of the critically ill infant.
The adult and fetal circulation differs in many ways. The fetal circulation is distinguished by (1) the placenta as the organ of respiration, (2) high pulmonary vascular resistance (PVR), (3) low systemic vascular resistance (SVR), and (4) fetal ventricles that pump in parallel with right ventricular dominance. While the fetus lives in a low oxygen environment, the oxygen content of the blood of the fetus is similar to that of adults (20 mL of oxygen/100 mL of blood) because of a higher concentration of hemoglobin that has high affinity for oxygen. The neonatal circulation has several shunts—the ductus arteriosus, ductus venosus, and foramen ovale—that direct more oxygenated blood to the brain and heart and bypass the lungs. Changes then occur that allow the parallel circulation of the fetus to convert to the series circulation of the adult:
With the first breath, expansion of the lung, increased alveolar oxygen, an increase in pH, and neurohumoral mediators and nitric oxide (NO) relax the pulmonary vasoconstriction.
When the placenta separates from the uterine wall, the placental blood vessels constrict, and SVR and left ventricular afterload increase. The decrease in PVR plus increase in SVR raises left atrial pressure above right atrial pressure (RAP) and functionally closes the “flap valve” of the foramen ovale. The foramen ovale may not close anatomically for months to years, if ever. It is patent in at least 15% of adults.
The decrease in PVR causes flow through the ductus arteriosus to reverse. This exposes the ductus to oxygenated systemic arterial blood, which along with the rapid decrease in prostaglandin E 2 after birth closes the ductus. Anatomic closure of the ductus requires several weeks.
The ductus venosus closes passively with removal of the placental circulation and readjustment of portal pressure relative to inferior vena cava pressure.
There is a further gradual decline in PVR secondary to structural remodeling of the muscular layer of the pulmonary blood vessels. During fetal life, the central pulmonary vascular bed has a relatively thick muscle layer. After birth, the muscle coat thins and extends to the periphery of the lung—a process that takes months to years to complete.
The functional integrity of autonomic circulatory control during fetal and perinatal development is still a matter of considerable speculation. The fetal heart has reduced catecholamine stores and increased sensitivity to exogenously administered norepinephrine (NE).
Adrenergic innervation of the human myocardium is complete between 18 and 28 weeks’ gestation. Human newborns have low cardiac stores of NE and decreased numbers of sympathetic nerves after birth. Adrenergic responses are apparently present but diminished in newborn humans. In human neonates, the cholinergic system is completely developed at birth, and the heart is sensitive to vagal stimulation. Bradycardia is the probable response to an increase in autonomic tone. The baroreceptor reflex is present but incompletely developed at term in humans. In preterm infants, postural changes elicit no change in HR, suggesting an incomplete or attenuated baroreceptor response. The chemoreceptor response is well developed in utero. The fetal bradycardia that occurs in response to hypoxia is thought to be mediated through chemoreceptors and may be similar to the oxygen-conserving mechanisms of diving animals.
Fetal myocardial metabolism differs from that of adults. Relative “hypoxia” is normal in utero, and infant hearts tolerate hypoxia better than the hearts of adults do. This difference may be due in part to high concentrations of glycogen in fetal myocardial tissue and to the ability to more effectively use anaerobic metabolism. Because of the high glycogen stores and the ability to use anaerobic metabolism efficiently, the fetal/newborn heart is relatively resistant to hypoxia and can be resuscitated more easily if oxygenation and perfusion are reestablished reasonably quickly.
Oxygen consumption increases precipitously after birth, presumably because neonates are required to maintain their own temperature. A full-term infant’s oxygen consumption in a neutral thermal environment is approximately 6 mL/kg/min; it increases to 7 and 8 mL/kg/min at 10 days and 4 weeks, respectively.
Congenital heart disease causes significant alterations in oxygenation, perfusion, and myocardial function after birth ( Box 79.1 ). These abnormalities can be divided into hypoxic and normoxic lesions. The latter include obstructive lesions of the left side of the heart (mitral valve stenosis, aortic valve stenosis, aortic stenosis, anomalous pulmonary venous return, ventricular septal defect, or patient ductus arteriosus with a right-to-left shunt), whereas hypoxic lesions include tricuspid valve stenosis, pulmonary valve stenosis, pulmonary artery stenosis or aplasia, and the tetralogy of Fallot. Right-sided lesions cause hypoxia if the left-to-right shunting of blood is sufficient to cause congestive heart failure (CHF) and pulmonary edema. Newborns with significant congenital heart disease commonly have either cyanosis or CHF. The degree of dysfunction usually changes during the first few months of life as PVR decreases to adult levels. As PVR decreases, left-to-right shunting of blood usually increases, and the symptoms of CHF become more apparent. Many neonates with a significant ventricular septal defect, which may or may not be observed during the preoperative workup, have no left-to-right shunting for several weeks after birth; however, induction of alkalosis during surgery can increase shunting. In the newborn, the usual signs and symptoms of CHF include poor feeding, irritability, sweating, tachycardia, tachypnea, decreased peripheral pulses, poor cutaneous perfusion, and hepatomegaly. Many patients with pulmonary edema exhibit tachypnea without retractions. Cyanosis occurs with structural cardiac disease, but other causes such as respiratory disease, increased PVR (persistent pulmonary hypertension), and methemoglobinemia must also be considered. Congenital heart disease is diagnosed by physical examination, electrocardiogram (ECG), chest radiograph, and echocardiogram, postnatally and via fetal echocardiography. Cardiac catheterization is occasionally performed as interventional therapy or as a diagnostic tool. Magnetic resonance imaging (MRI) is used to define the anatomy of congenital heart lesions before cardiac surgery. Initial treatment of congenital heart disease is aimed at relieving CHF, improving systemic perfusion, and improving or maintaining pulmonary blood flow. The ductus arteriosus must be maintained open in instances of hypoplastic left heart syndrome, aortic stenosis or atresia, interrupted aortic arch, and symptomatic neonatal coarctation of the aorta. In many cases, infusion of PGE 1 sustains life until definitive surgical correction can be performed.
Cyanotic congenital heart lesions
Tetralogy of Fallot
Transposition of the great arteries
Hypoplastic left heart syndrome
Pulmonary atresia with an intact ventricular septum
Single ventricle
Total anomalous pulmonary venous return
Tricuspid atresia
Congenital heart lesions manifested as congestive heart failure
Ventricular septal defect
Patent ductus arteriosus
Critical aortic stenosis
Coarctation of the aorta
Shock is the inability to provide adequate oxygen to the tissues that require it. The condition of shock depends on the balance of supply and demand of oxygen. Typically the body delivers excess oxygen to the tissues. Under periods of stress or illness there can be a decrease in supply caused by diminished blood flow or as decreased oxygen in blood. There can also be increased demand or oxygen extraction from the tissues. The content of oxygen is the blood is dependent on the amount bound to hemoglobin and the amount dissolved in plasma. Oxygen content (CaO 2 ) (mL/dL) = (1.34g/dL) (SaO 2 ) (Hb) + (PaO 2 ) (0.003). The normal oxygen content is approximately 20 mL/dL. Delivery of oxygen to the tissues depends on oxygen content and cardiac output. Oxygen delivery (
) (mL/min) = oxygen content (CaO 2 ) × cardiac output (CO) × 0.01. Oxygen consumption (
) is the demand portion of the equation. Oxygen consumption (
) is independent of oxygen delivery (
) above a critical threshold and over a wide range. Below this critical threshold
is dependent on
. For infants and young children,
is estimated at 175 mL/min/m 2 . Oxygen consumption is equal to oxygen delivery multiplied by oxygen extraction (O 2 EX) by the body:
. Oxygen extraction O 2 EX is equal to (CaO 2 – CvO 2 )/CaO 2 . CaO 2 is the oxygen content of arterial blood and CvO 2 the oxygen content of venous blood. The difference between oxygen content of arterial and venous blood is predictably 4 to 6 mL/100 mL blood. Initially, as oxygen delivery decreases, the oxygen consumption can remain constant via increased extraction. Below a critical threshold in oxygen delivery, oxygen consumption becomes dependent on delivery. When oxygen to meet metabolic needs of the body cannot be met, nonessential metabolism is decreased or eliminated. Such metabolism includes growth, neurotransmitter synthesis, thermoregulation, and so forth. In this way the remaining oxygen can continue to be substrate for mitochondria. There are organs in the body, such as the kidney, skin, intestines, and skeletal muscle, that receive a high supply of blood relative to their metabolic needs. These organs also have a high proportion of sympathetic nerve innervations that allow for redistribution of blood flow to organs that with limited oxygen reserves such as the brain and heart.
There are several schemas which clinicians use to classify shock. Further within these classification schemas, disease states can fall into more than one category. One classification schema separates shock into the categories of hypovolemic, cardiogenic, distributive or vasogenic, and extracardiac obstructive.
Hypovolemic shock can be due to hemorrhage from trauma or gastrointestinal (GI) losses from internal bleeding. Nonhemorrhagic hypovolemic shock can be due to external losses of fluid from vomiting, diarrhea, polyuria, and poor fluid intake. Fluid redistribution in cases of burns, trauma, and anaphylaxis can also be a cause.
Cardiogenic shock may be myopathic due to decreased heart function. For adults this may commonly follow myocardial infarction. For children, myocarditis or cardiomyopathy are more common. Other causes of cardiogenic shock include mechanical failure such as valvular regurgitation or obstruction. Significant arrhythmias may result in cardiogenic shock when contractions are so asynchronous they decrease cardiac output.
Extracardiac obstructive shock results from a physical obstruction that prevents adequate forward circulatory flow. Causes include inadequate preload secondary to mediastinal masses, increased intrathoracic pressure from tension pneumothorax, constrictive pericarditis, and cardiac tamponade from pericardial effusions. Pulmonary hypertension, pulmonary embolus, and aortic dissection can cause obstruction to systolic contraction.
Distributive shock is caused by a decrease in SVR and the maldistribution of end-organ blood flow. Cardiac output may be increased in distributive shock, however, blood pressure may remain low due to a very low SVR. Septic causes of distributive shock can be related to bacterial, fungal, viral or rickettsial infections or toxins produced from these infections. Toxic shock syndrome would be an example of toxin-mediated hypotension. Anaphylactic or anaphylactoid reactions are a type of distributive shock. Systemic inflammatory response syndrome (SIRS) may present with distributive shock. Spinal shock can result in distributive shock on a neurogenic basis. Adrenal insufficiency with low circulating hormones results in distributive shock decreased SVR.
Maintaining a high index of suspicion is important to rapidly identify shock in pediatric patients. Volume losses may be readily apparent from the history of present illness. Fever, rash and irritability may point to infection. However, cardiogenic shock may present with vague reports of decreased activity and level of alertness. In addition, if the patient’s shock is currently compensated, changes in physical findings may be limited. A child in shock may present initially with tachycardia, cold extremities, and poor capillary refill. Further, in distributive shock, the child may be warm with just an isolated tachycardia. A brief pertinent physical exam should evaluate level of alertness, peripheral perfusion, mucous membranes, pulse rate and quality, respiratory effort, urine output, and blood pressure. In children, blood pressure may be preserved until the degree of shock has progressed. Hypotension is a sign of late and decompensated shock in children. Metabolic acidosis may not be present on the initial laboratory tests.
The body applies compensatory mechanisms with the onset of shock to maintain adequate tissue perfusion for as long as possible. There is redistribution of fluid from the intracellular and interstitium to the vascular space. There is a decrease in glomerular filtration to limit renal fluid losses. Renal fluid losses are also limited by the release of aldosterone and vasopressin. There is an increase in sympathetic activity and release of epinephrine. This results in decreased venous capacitance and some preservation of blood pressure. HR is increased as the body tries to maintain cardiac output. There is an increase in cardiac contractility through circulating catecholamines and adrenal stimulation. Increase in sympathetic nerve stimulation shunts blood away from nonvital organs. At the tissue level, transfer of oxygen from hemoglobin is increased by increased red blood cell (RBC) 2, 3-diphosphoglycerate, fever, and tissue acidosis.
Aggressive therapy to treat pediatric septic shock appears to have resulted in improved outcomes. Therefore therapy for septic shock appears to be a good model for the treatment of shock in general. The overall goal of therapy in shock is to treat the underlying cause, return adequate oxygen delivery to the tissues, and remove metabolic products that developed during anaerobic metabolism. It appears the faster the body returns to adequate perfusion, the better the overall outcome. Many hospitals have developed sepsis pathways based on the data presented as follows that act as guidelines for resuscitation and are readily available to all care providers ( Fig. 79.1 ).
In 1991 Carcillo et al. described a population of 34 children that presented with septic shock to an emergency department. Shock was diagnosed based on hypotension for age, with decreased perfusion, poor peripheral pulses, cool extremities, and tachycardia. Sepsis was defined as a positive blood or tissue culture. Remarkably, within 6 hours of presentation, all the patients had a pulmonary artery catheter placed. The overall mortality for the group was 47%. However, in the nine patients who received more than 40 mL/kg of fluids in the first hour, there was only one death (mortality 11%). The authors point out this patient died with a second episode of sepsis 2 weeks later. In this study, the rapid fluid administration was not associated with an increase in cardiogenic pulmonary edema or ARDS.
In 2001 Rivers et al. published a study in adult patients with septic shock showing early, aggressive, goal directed therapy in the first 6 hours of care improved mortality. There were 263 adults were enrolled; 133 received standard therapy based on clinician discretion. The 130 patients randomized to early goal-directed therapy followed protocols treating hypovolemia and supporting blood pressure with vasoactive agents if necessary. The baseline characteristics of the two groups were similar. The in-hospital mortality was 46.5% in the standard therapy group and 30.5% in early goal-directed therapy group ( P < .01). Although in adults, this demonstrated the need for early aggressive intervention.
Following the Rivers publication, a task force was formed by members of the Society of Critical Care Medicine to address shock in children. Their work was published in 2002 as “Clinical Practice Parameters for Hemodynamic Support of Pediatric and Neonatal Patients in Septic Shock.” Their guidelines were incorporated into the American Heart Association’s (AHA) Pediatric Advanced Life Support (PALS) Provider Manual. Their guidelines were translated into Spanish and Portuguese and disseminated widely. The effectiveness of these interventions as well as an 2007 update was published by the same group in 2009. They highlighted significant improvements in mortality in dengue shock syndrome, malaria, and septic shock treated by community physicians using early goal directed therapy. The guidelines include rapid recognition of shock and early antibiotic administration and early administration of intravenous (IV) crystalloid. The initial resuscitation should include 20 mL/kg of isotonic saline or colloid pushed as a bolus to over 60 mL/kg until there is an improvement in the patient’s perfusion or rales or hepatomegaly develops. The goal is for the initial fluid resuscitation to occur in the first 15 minutes of therapy, and therapy should be initiated even if peripheral IV cannulation attempts fail, by placing and intraosseous (IO) device ( Fig. 79.2 ). The guidelines target therapeutic end points of normal pulses with no difference between peripheral and central; capillary refill ≤ 2 seconds; warm extremities, normalization of blood pressure for age, mental status, glucose concentration, ionized calcium concentration; and urine output greater than 1 mL/kg/h. If central venous access is not readily obtained, consideration should be given for placement of an IO line. Cold shock (cold mottled extremities with prolonged capillary refill) should be treated with dopamine up to 10 μg/kg/min and then epinephrine 0.05 to 0.3 μg/kg/min if there is no improvement. Warm shock (brisk capillary refill) should be treated with NE. Arrangements should be made early to admit the child to an ICU. If shock is not reversed with the inotropic support, hydrocortisone should be considered for catecholamine resistant shock. Recommendations for stabilization in the ICU following the first hour of therapy include monitoring central venous pressure, central venous saturation, and cardiac output. Persistent shock that is resistant to catecholamines should prompt the clinician to rule out pericardial tamponade, pneumothorax, or significantly elevated intra-abdominal pressure that may be compromising circulation. In the absence of a correctible condition, extracorporeal membrane oxygenation (ECMO) should be considered.
There were several new recommendations in the 2007 guidelines that addressed changes in the literature between 2002 and 2007. It was identified that the availability of skilled practitioners to place central venous access could delay the initiation of inotropic support. Therefore, the 2007 guidelines recommended the use of a peripheral IV dopamine or epinephrine if there was delay in obtaining central venous access. Ongoing monitoring of the access site should be performed. It was not recommended to use NE in a peripheral IV, due to risk of extravasation. In the 2002–2007 interval there were several pediatric and adult studies indicating adrenal suppression and increased severity of illness adjusted mortality with the use of etomidate. The 2007 guidelines do not recommend the use of etomidate unless it is in the format of a randomized controlled trial. Ketamine with atropine was recommended for sedation for invasive procedures in infants and children. However, due to limited experience, ketamine could not be recommended for the newborn population.
The 2007 guidelines recommend titrating therapy to cardiac output and indicate that there are several methods by which cardiac output can be measured. The use of pulmonary arterial catheters has decreased in pediatrics over time, but other methods are available. A good review of monitoring techniques was published by Mtaweh et al. in 2013. Cardiac output can be monitored by newer techniques analyzing the arterial pulse wave, transpulmonary thermodilution, carbon dioxide rebreathing, echocardiography, bio-impedance of the thorax, and ultrasound continuous-wave Doppler. These techniques are less invasive than pulmonary artery catheters. However, many still require validation studies in pediatric, and they may not be available at all centers.
One additional area to be addressed in the 2007 guidelines is in the area of fluid removal. A study published by Goldstein et al. in 2005 in pediatric patients with multiorgan failure, including acute renal failure requiring continuous renal replacement therapy (CRRT), showed improved survival in the group that had a lower percentage of fluid overload at the initiation of CRRT. While supporting the primary premise of fluid resuscitation, the 2007 guidelines offered new recommendation for fluid removal in patients with fluid overload and multiorgan failure. They recommended the use of diuretics, peritoneal dialysis, or CRRT in patients who had been adequately fluid resuscitated but were not able to maintain an even fluid balance through native urine output. Again, it should be noted that peritoneal dialysis and CRRT for pediatric patients may not be available at all centers. However, the association between fluid overload and mortality with acute renal failure has been seen in other studies and will likely be an ongoing issue in pediatric ICU care.
The concern for possible adrenal insufficiency during septic shock needs to be addressed by the clinician caring for the patient. There are certain instances where limited function of the adrenal axis is anticipated. This would include patients who have recently received glucocorticosteroids, ketoconazole, or etomidate. Further, patients with disease states such as purpura fulminans or those affecting the hypothalamus, pituitary, or adrenal glands will be at increased risk. Patients with adrenal insufficiency need supplemental corticosteroids. However, for children with septic shock but without these factors, it is not clear whether the risk of relative adrenal insufficiency or treatment with systemic steroids alter outcome. Dr. Zimmerman reviewed the adult and limited pediatric literature in 2007 for therapeutic steroid use in sepsis. He highlighted adult studies showing high dose short courses of steroids are associated with decreased survival. Further, data from the CORTICUS trial indicated that low dose steroids as a physiologic replacement during periods of vasopressor resistant shock resolve shock more quickly but there was no change in mortality. In turn, the 2007 guidelines were unchanged from 2002. Hydrocortisone treatment was only recommended for patients with absolute adrenal insufficiency or adrenal-pituitary axis failure and catecholamine-resistant shock. Absolute adrenal insufficiency was defined as peak cortisol concentration of less than 18 μg/dL obtained after corticotropin stimulation.
Pharmacologic support of the circulation includes positive inotropic and chronotropic agents, vasoconstrictors and vasodilators (afterload reduction), and antiarrhythmics (see Chapters 14, 18, and 86). Most currently used drugs have not been adequately tested in children, so dosage recommendations and anticipated effects must be extrapolated from adult doses and clinical experience.
Positive inotropic drugs are used to augment the cardiac output of patients with circulatory failure. Most inotropic agents also affect the HR and vasomotor tone. Tachycardia in a child is usually well tolerated and is frequently beneficial. In a neonate whose ventricles are relatively noncompliant and whose stroke volume is less variable, tachycardia is an important means of augmenting cardiac output. Because drugs that increase the HR or contractility also increase myocardial oxygen consumption, adequate arterial oxygenation and sufficient metabolic substrates are required when these drugs are administered. The cardiovascular response to sympathomimetic amines is attenuated in the presence of severe acidosis and possibly sepsis; higher infusion rates of these drugs are required and need readjustment as the acidosis improves. Commonly used inotropes are listed with brief comments regarding their use in pediatric intensive care are provided in the following paragraphs ( Table 79.1 ).
Drug | Effect | Dose (μg/kg/min) | Inotropy | Chronotropy | Vasodilation | Vasoconstriction |
---|---|---|---|---|---|---|
Epinephrine (Adrenalin) | α, β | 0.05-2.0 | ++ | ++ | ++ | |
Isoproterenol (Isuprel) | β 1 , β 2 | 0.05-2.0 | ++ | ++ | + | |
Dopamine (Intropin) | δ | 1-3 | +Renal splanchnic | |||
β > α | 5-15 | + | + | + or − | ||
β, α | >15 | + | + | + | ||
Milrinone | Bolus: 50 μg/kg over 15-min period | + | + | |||
Infusion: 0.375-0.75 | ||||||
Norepinephrine | α >> β | 0.05-1.0 | Slight+ | + | ++ | |
Nitroprusside | 0.5-10 | ++ | ||||
Arterial > venous | ||||||
Nitroglycerin | 1-20 | ++ |
Epinephrine is useful for the treatment of shock in the presence of myocardial dysfunction. Typical starting doses in children are 0.05 to 0.2 μg/kg/min; with escalating doses up to 1 to 2 μg/kg/min, there is profound vasoconstriction in the periphery and abdominal organs to shunt blood to the heart and brain.
Dopamine is the most commonly infused inotrope in pediatric patients. Dopamine is the metabolic precursor of both NE and epinephrine. Its effects are dose dependent, with dopaminergic activity at low doses (although these low-dose dopamine effects have not been demonstrated in critically ill children); β-adrenergic activity with intermediate doses 5 to 10 μg/kg/min exhibiting chronotropic and inotropic effects; and some α-adrenergic activity at higher doses, with 10 to 20 μg/kg/min exhibiting peripheral vasoconstriction. Young children require higher doses of dopamine than adults do to produce the same effect. In one study, an infusion of 15 μg/kg/min was required to increase cardiac output above control levels after cardiac surgery. This may reflect the decreased releasable myocardial stores of NE in immature ventricles. Therefore, in the sick preterm infant there can be decreased dopamine clearance with a much greater vasopressor response than expected.
Vasopressin is a pituitary peptide hormone with method of action on the kidney and vasculature. In the kidney, vasopressin controls water reabsorption in the renal tubules, and in the vasculature, it causes vasoconstriction by stimulating smooth muscle V1 receptors. Its clinical applications include GI hemorrhage, central diabetes insipidus (DI), and as a second- or third-line agent to treat hypotension.
Isoproterenol is a synthetic, potent, nonselective β-agonist with strong chronotropic effects with very low affinity to α-adrenergic receptors, and is usually well tolerated in children. However, high doses of isoproterenol can cause myocardial ischemia. Isoproterenol also induces vasodilation that is responsive to acute volume administration. It is often used for increasing HR in complete heart block, in the immediate postoperative period after cardiac transplantation to improve cardiac output by increasing HR in the denervated donor heart, and as a potent pulmonary vasodilator during pulmonary hypertensive crisis via β2-adrenergic receptor activity.
Dobutamine provides positive inotropy and afterload reduction, β and α receptors. Its function is primarily as a inotropic agent but with less vasopressor activity compared with dopamine. It is only used as a continuous infusion of 5 to 20 μg/kg/min, and in some studies may increase myocardial oxygen In children but not in adults it causes tachycardia.
NE, a drug with strong α- and β-agonist effects, has had a resurgence of use in infants and children. Children with nearly normal cardiac function and marked peripheral vasodilation have good responses to this drug. It is especially useful in instances of warm septic shock, anaphylaxis, liver failure, and sympathetic blockade with regional anesthesia. It will increase SVR, but also limits mesenteric blood flow, including hepatic perfusion.
Milrinone is a selective phosphodiesterase III inhibitor that increases cyclic adenosine monophosphate by inhibiting breakdown. Milrinone has both inotropic and vasodilator effects, without acting on α and β receptors. This drug has improved the outcome of children who have low cardiac output syndrome after cardiac surgery. The loading dose of milrinone is 25 to 75 μg/kg administered over a period of 10 minutes; the maintenance infusion rate is 0.25 to 0.75 μg/kg/min. Loading doses are often avoided in the ICU setting because of resultant hypotension. Renal failure significantly increases the elimination half-life of this drug. Outside the cardiac ICU, milrinone is used for vasoconstricted septic shock and may have a role in the treatment of pulmonary hypertension.
Levosimendan is a novel agent that increases the sensitivity of the contractile apparatus to calcium increasing inotropy by binding to cardiac myocyte troponin C. This agent will increase cardiac ejection fraction, while reducing catecholamine dose with minimal effects on blood pressure and HR. In children, the most common indications have been for cardiac failure or post–cardiac surgery, with a loading does of 612 μg/kg followed by an infusion of 0.1 to 0.2 μg/kg/min.
Nesiritide is a recombinant form of the human B-type natriuretic peptide, the hormone release from the cardiac ventricles in response to volume overload and increasing mechanical wall stress. The action is on guanylate cyclase with resulting venous and arterial vasodilation. In addition, B-type natriuretic peptide leads to myocardial relaxation (lusitropy) and natriuresis. In children, it has been used to decrease central venous pressure and increase urinary output. Usual dosing suggestions for children and adults: initial 2 μg/kg bolus followed by a continuous infusion of 0.005 to 0.01 μg/kg/min.
Digitalis is useful for the long-term treatment of myocardial failure in children but may not be effective in neonates. Because of its long half-life and unpredictability, digitalis should be administered cautiously to children who have changing levels of serum potassium, calcium, and pH. In these cases, it is more appropriate to use rapid-acting, titratable inotropic agents.
When serum ionized calcium levels are below normal, administration of calcium produces a positive inotropic effect. If the patient’s ionized calcium levels are normal, less marked inotropic effects occur. Low ionized calcium levels most commonly occur in patients with DiGeorge’s syndrome, when large volumes of citrate-containing blood products are rapid administered, and in neonates with relatively unstable calcium metabolism. Calcium also has effects on the cardiac conduction system. Rapid administration of calcium can cause severe bradycardia or asystole. This effect may be exaggerated in hypokalemic children or in those receiving digitalis. The vasomotor effects of calcium are controversial, but most reports show an increase in both SVR and PVR when the drug is administered.
Severe acidosis decreases myocardial function and tissue perfusion. Correction of acidosis with 1 to 2 mEq/kg of sodium bicarbonate is indicated for a pH below 7.20 if ventilation is adequate (PCO 2 <40 mm Hg if possible). Treatment is necessary because the circulatory system is refractory to sympathomimetic amines when the pH is less than 7.00. After initial correction of pH, persistence or reappearance of metabolic acidosis suggest a continuing underperfused state and the need for further therapy. Administration of sodium bicarbonate is only a stopgap measure to improve the response to drugs. Repeat infusions of sodium bicarbonate can cause hypernatremia and hyperosmolarity. Every 50 mEq of bicarbonate administered produces 1250 mL of CO 2 when the bicarbonate is fully reacted with acid. Consequently, adequate ventilation must be ensured while the drug is administered to avoid worsening the acidosis. Trishydroxymethylaminomethane (THAM) is an alternative to sodium bicarbonate, but larger volumes of THAM are required to produce the same amount of acid-base correction, which may be a problem in patients who have CHF. THAM does not increase PaCO 2 .
Vasodilators are used to control systemic hypertension, increase cardiac output by decreasing afterload, control pulmonary hypertension, and control cardiac shunting. Vasodilators are an effective treatment of systemic hypertension and increase cardiac output in children with CHF. Treatment of pulmonary hypertension and intracardiac shunting with vasodilators has met with limited success because they decrease both PVR and SVR, which may increase extrapulmonary right-to-right shunting and further reduce pulmonary blood flow.
Nicardipine is a dihydropyridine calcium channel-blocking agent used as an IV infusion that has powerful, antihypertensive effects in children. Studies have shown that the rapid onset of action is usually within 1 minute, adding to the profile appropriate for treating severe hypertension. Flynn et al. reports that nicardipine is an effective anti-hypertensive medication in children ranging in age from 2 to 18 years. In our institution, nicardipine is the drug of choice for hypertensive crisis. Infusion ranges: 0.5 to 1.0 μg/kg/min up to 3.0 μg/kg/min.
Sodium nitroprusside relaxes arteriolar and venous smooth muscle, which decreases afterload and preload. The half-life of sodium nitroprusside is only minutes, making it safe to titrate the drug to a desired effect. Nitroprusside is commonly used to control severe systemic hypertension, to provide controlled hypotension to reduce blood loss, and to increase cardiac output in children with low cardiac output syndromes (myocarditis, post–cardiac surgery status). Sodium nitroprusside can generally be used for days without problems, although cyanide and thiocyanate poisoning develops in some children, especially those with renal failure or reduced renal perfusion. Serum thiocyanate levels of 10 mg/dL are associated with weakness, hypoxia, nausea, muscle spasms, and disorientation. When these symptoms occur, nitroprusside administration should be discontinued immediately.
Hydralazine is used to control systemic hypertension because it relaxes arterial smooth muscle more than it relaxes veins. Administration of the drug can cause headache, nausea, dizziness, sweating, and tremors. The most important acute side effect is tachycardia, which may increase cardiac output; labetalol, a β-antagonist, can counteract this effect.
These competitive α-adrenergic blockers have had varied success in the treatment of pulmonary hypertension. However, they are effective in treating the symptoms of pheochromocytoma preoperatively. Serious side effects of these drugs include tachycardia, ventricular arrhythmias, hypotension, and tissue edema.
PGE 1 acts directly on vascular smooth muscle and has greatly improved the care of neonates with heart disease. At infusion rates of of 0.1 μg/kg/min, patency of the ductus arteriosus is maintained and a closed ductus reopens in some neonates. The drug is indispensable in the care of patients with ductus-dependent cardiac lesions, such as interrupted aortic arch, critical aortic stenosis, or hypoplastic left heart syndrome, where systemic blood flow is supplied through the ductus arteriosus. It is equally important for the care of patients who have pulmonary atresia or critical pulmonic stenosis. Apnea, fever, and hypotension are common side effects of this drug.
NO is an endothelium-derived relaxing factor that selectively vasodilates the pulmonary vasculature. When administered by inhalation to patients with pulmonary hypertension, NO reduces PVR. It improves the survival of neonates who have reactive pulmonary hypertension. This compound is inactivated by hemoglobin before it reaches the systemic circulation. On rare occasions, NO causes systemic vasodilation or clinically significant methemoglobinemia when administered at 5 to 80 ppm.
Sinus tachycardia or an elevated HR for age is not considered an arrhythmia. However, patients with a significantly increased HR may be the most critically ill in the ICU. Causes of tachycardia include hypovolemia, fever, pain, anxiety, CHF, myocardial disease and dysfunction and thyrotoxicosis. With all of these causes, the goal is to treat the underlying disease state and not the tachycardia. For children without underlying heart disease, temporary increases in HR up to 180 to 200 beats/min is well tolerated. This is also not uncommon; children cannot increase their stroke volume so they increase their cardiac output by increasing their HR. Again, the goal is not to specifically control an elevated HR but to treat the cause of the tachycardia. Sinus arrhythmia is a phasic acceleration and slowing of the HR that occurs with respiration. This is not an uncommon finding. It indicates that the patient has a vagal tone greater than sympathetic tone and it can indicate that there is good cardiac reserve. A slow HR or sinus bradycardia is another relatively common heart rhythm seen in the ICU. It is an unremarkable finding in an older teenage patient who is relatively fit. Other potential causes can include increased intracranial pressure (ICP), hyperkalemia, hypothermia, profound hypoxia, and hypothyroidism. These causes should also be investigated. A slow HR is being seen more commonly with the increased of Dexmedetomidine but can also occur with beta blockers or Digoxin use. Sinus node dysfunction can occur following repair of congenital heart disease in children. Temporary slowing may be treated with the transcutaneous pacemaker placed during surgery. In the absence of myocardial pacing, if there is complete heart block or a very slow ventricular escape rate, a pacemaker may be needed shortly after the cardiac surgery. Otherwise, some amount of time is given to see if this will resolve.
Normal cardiac conduction starts in the sinus node. The electrical activity propagates through the internodal pathways in the atrium, is delayed in the AV node, it travels though the bundle of His, and then is conducted to the ventricles through the left and right bundle branches. Supraventricular tachycardia (SVT) is an elevated HR occurring at the level of the atrium, the AV node, or both. SVT typically has a narrow QRS morphology. Sinus tachycardia is therefore not a type of SVT but an acceleration of the normal conduction pathways. SVT includes reentrant and non-reentrant tachycardias.
The reentrant tachycardias include AV node reentrant tachycardia (AVNRT), orthodromic reciprocating tachycardia (ORT), and atrial flutter. AVNRT is what is classically thought of as pediatric SVT. The reentrant tachycardias occur due to the presence of an accessory conduction pathway that allows for abnormal electrical conduction in the heart. The presence of the abnormal pathway may be apparent on a standard ECG such as the case of Wolf-Parkinson-White (WPW). Alternatively the abnormal pathway may not appear on an ECG and is described as a concealed pathway. Concealed pathways are non-WPW ORT. In AVNRT, the AV node itself is the area in which the reentrance occurs. In atrial flutter there is a micro-reentrant circuit within the atrial tissue itself. In children, the circuit is typically near the tricuspid valve. In atrial flutter, after the reentrant circuit in the atria, the conduction proceeds through the AV node, where it is slowed. The reentrant circuit is small, and the rates of atrial flutter can be very high. As the conduction is slowed in the AV node, these high rates are not usually conducted to the ventricle. However, if atrial flutter or fibrillation occurs in a patient with WPW, the accessory pathway can allow conduction of the electrical impulse at a rate much greater than through the AV node. This can lead to ventricular tachycardia or fibrillation and can cause sudden death.
The non-reentrant causes of SVT occur due to abnormal automaticity of myocardial tissue. Causes of abnormal automaticity include atrial fibrillation and ectopic atrial tachycardia (EAT). In non-reentrant SVT, the elevated atrial rate is slowed as conduction goes through the AV node. In children, atrial fibrillation is caused by disorganized circuits typically near the pulmonary veins. This rhythm is described as irregularly irregular. EAT is rapid atrial beats that are consecutive and occur without sinus morphology. There can be one focus of the rapid atrial beats. Alternatively, in multifocal or chaotic atrial tachycardia, there can be several different atrial origins. Brief periods of EAT usually do not cause much sequel but can lead to cardiomyopathy if it is prolonged.
Treatment of reentrant SVT is based on whether the patient is clinically unstable or stable. The abnormal reentrant circuit can be interrupted with synchronized cardioversion or other methods. If the patient is unstable, reentrant SVT is treated with synchronized cardioversion with a dose of 0.5 to 1 J/kg. If the patient is stable, there is time to try other therapies. Therapies that increase vagal tone such as ice to the eyes or a Valsalva maneuver may interrupt the reentrant circuit. The medication adenosine will temporarily block conduction through the AV node. Adenosine can be used to interrupt episodes of reentrant SVT that have a reentrant circuit using the AV node. If the reentrant circuit does not include the AV node adenosine might not stop the tachycardia, but it may be helpful with diagnosis. Following administration of adenosine, there will be a period of sinus pause. Adenosine is metabolized by erythrocytes so it is a short acting medication. Equipment to perform cardioversion should be immediately available when adenosine is given. The initial dose is 0.1 mg/kg, and the dose should be given quickly with a sufficient flush. It is more effective when given centrally if available. If it is not effective at the dose of 0.1 mg/kg, the second dose can be increased to 0.2 mg/kg. Higher doses than this are not likely to be more effective, and if the SVT persists, other medications such as amiodarone, procainamide, or verapamil may be necessary. Amiodarone can block an accessory pathway as well as the AV node. If given too quickly, amiodarone will decrease the blood pressure. For both amiodarone and procainamide, continuous infusions may be necessary after the loading dose. Verapamil will block the AV node for a much longer period of time than adenosine. However, in younger patients (<2 years), verapamil may induce other life-threatening arrhythmias. If a patient has SVT, a cardiology consult should be obtained. This is because an echocardiogram may be beneficial, and depending on the cause, there may be a need for long-term follow-up.
Junctional ectopic tachycardia is caused by abnormal automaticity in an area around the atrioventricular junction. This is not a common pediatric arrhythmia but can occur following repair of congenital heart disease. The most common lesion with which this occurs is tetralogy of Fallot.
Wide complex tachycardias are assumed to arise from the ventricle until proven otherwise. SVT can cause a wide complex tachycardia if there is aberrancy of the conduction through the pathways in the ventricle. However, given the risk of delaying therapy, all wide complex tachycardias should initially be treated as ventricular tachycardia. If there is no pulse, initiate CPR, defibrillate, and follow PALS guidelines. If the patient has a pulse and stable blood pressure, there may be time to consider other therapies. These therapies are cardioversion or use of medications such as adenosine, amiodarone, or procainamide. Ventricular fibrillation is treated with CPR, defibrillation, and then medications following PALS guidelines. Ventricular rhythms should be quickly examined for the possibility of Torsades de Pointes, as giving magnesium will be especially helpful.
In the course of following the continuous rhythm strip of all children in the PICU, common abnormalities may be noted. A prolongation of the PR interval or first degree heart block can occur in otherwise normal children. Typically, these children are asymptomatic. Second-degree heart block occurs as Mobitz Type I and Mobitz Type II. Mobitz Type I is also known as Wenckebach . This is a gradual prolongation of the PR interval until a QRS is not seen and then the cycle restarts. This occurs due to delay of the electrical signal in the AV node, and it can be a benign phenomenon. Mobitz Type II is less likely to be a benign phenomenon. The PR interval remains constant, but intermittently there is no QRS or ventricular beat. This phenomenon is evidence of disease of the His-Purkinje fibers and can progress to complete heart block. Mobitz Type II occurs much less frequently in children as compared with adults. Complete heart block or third-degree AV block is the complete dissociation of atrial and ventricular activity. In complete heart block, the atria contract at a rate greater than the ventricle. Ventricular contraction occurs through ventricular escape. Congenital complete heart block can occur in infants born to mothers who have an autoimmune disorder such as lupus. When there is damage to the conduction pathway during surgery for congenital heart disease, complete heart block can occur. As immediate treatment of complete heart block, the ventricular rate may be increased with IV isoproterenol. When this is ineffective, transthoracic or transvenous pacing will be necessary until definitive therapy can be arranged.
Premature beats are also seen quite frequently in a PICU setting. Premature atrial contractions are usually benign and are caused by automaticity of atrial tissue other than the sinus node. Premature ventricular contractions (PVC) are usually benign with a few considerations. The presence of a central venous catheter touching the heart may cause increased PVCs, and if present, the catheter should be pulled back. Electrolyte abnormalities; typically of potassium, magnesium, and calcium, may cause PVCs. The frequency of PVCs may improve as the electrolytes are corrected. Exogenous catecholamines may cause PVCs, and the frequency of PVCs may improve if the catecholamines can be decreased. Endogenous catecholamines may cause PVCs, and the frequency may be decreased if pain or anxiety is treated.
Essential hypertension is uncommon in children, but when it occurs, it is often associated with another disease process ( Box 79.2 ) and is frequently difficult to control. The acute onset of severe systemic arterial hypertension is a medical emergency that has the potential of causing cardiovascular decompensation, encephalopathy, seizures, and intracranial hemorrhage. In older children, the neurologic manifestations of hypertension are more likely to precede cardiovascular decompensation. Neonates with severe hypertension are frequently initially found to have CHF. Treatment of hypertension is tailored to the disease process, the absolute degree of hypertension, and the presence of cardiovascular or neurologic symptoms.
Acute glomerulonephritis (e.g., poststreptococcal, Henoch-Schönlein purpura)
Hemolytic-uremic syndrome
Chronic glomerulonephritis (all types)
Acute and chronic pyelonephritis
Congenital malformations (dysplasia, hypoplasia, cystic diseases)
Tumors (e.g., Wilms, leukemic infiltrate)
Post–renal transplantation status; also rejection
Oliguric renal failure
Trauma
Obstructive uropathy
After genitourinary surgery
Blood transfusions in children with azotemia
Coarctation of the aorta
Renal artery abnormalities (e.g., stenosis, thrombosis)
Takayasu’s disease
Pheochromocytoma
Neuroblastoma
Adrenogenital disease
Cushing syndrome
Hyperaldosteronism
Hyperthyroidism
Hyperparathyroidism
Intravascular volume overload
Sympathomimetic administration (e.g., epinephrine, ephedrine)
Corticosteroid administration
Rapid intravenous infusion of methyldopa
Immobilization (e.g., fractures, burns, Guillain-Barré syndrome)
Hypercalcemia (e.g., hypervitaminosis D, metastatic disease, sarcoidosis, some immobilized patients)
Hypernatremia
Stevens-Johnson syndrome
Increased intracranial pressure (any cause)
Dysautonomia
After resuscitation
Profound changes occur in the cardiovascular and respiratory systems at birth. Failure to successfully make these changes may result in death or central nervous system (CNS) injury. Consequently, someone capable of performing neonatal resuscitation must be present at every delivery. Wasting time finding someone to resuscitate the neonate may be disastrous for the infant. This section discusses the causes and effects of cardiorespiratory insufficiency at birth and the techniques of resuscitation. When possible, the recommendations of the American Academy of Pediatrics have been followed.
Guidelines for neonatal resuscitation have been issued by many organizations, including the AHA and the American Academy of Pediatrics.
Initial stabilization should begin with a rapid evaluation of the newborn to determine if the infant is term, breathing, or crying, and has a normal tone ( Table 79.2 ).
Clinical Condition | Intervention |
---|---|
Initial resuscitation | Clear infant airway Warm, dry, stimulate, position Evaluate HR, respirations, color |
HR > 100 beats/min, breathing, no cyanosis | Observation |
HR > 100 beats/min, but persistent respiratory distress or cyanosis | Clear airway SpO 2 monitoring Consider CPAP |
Apnea, gasping, or HR < 100 beats/min | Bag-mask PPV SpO 2 monitoring |
After initiation of resuscitation (PPV), HR > 100 beats/min, effective ventilation | Post-resuscitation care |
HR < 60 beats/min | Consider intubation Chest compressions Coordinate PPV |
HR = 60-100 beats/min | Continue with PPV SpO 2 monitoring |
Ongoing assessment consists of three signs: HR, respirations, and oxygenation. The preferred method for auscultation of HR is by auscultation. All of these vital signs should be determined within the first 30 seconds.
Proper positioning by placing the infant in the sniffing position is recommended, and the practitioner must try to avoid either underextension or hyperextension, both of which will obstruct the airway. Deep sucking should be avoided even in healthy, vigorous newborns, because of risks of vagal-mediated bradycardia. This does not apply to newborns who may have airway obstruction or the depressed infant with meconium (covered later in this section.)
During the initial resuscitation period, the goal temperature for the newborn is normothermia. The initial step is to dry the infant and warm the infant to a goal axillary temperature of 36.5°C. The goal for each neonate is euthermia. Infants wrapped in polyethylene from the neck down will avoid evaporative heat loss. Controlled hypothermia should only be attempted in select tertiary centers within hours after birth in infants with hypoxic-ischemic encephalopathy (HIE).
One of the recent changes in neonatal resuscitation in the 2011 Neonatal Resuscitation Program Guidelines is the recommendation of positive pressure ventilation (PPV) with room air, unless chest compressions or medications are needed during the resuscitation then the recommendation are still for PPV with 110% oxygen. It is important to place a preductal (right hand) oximeter probe on the newborn if PPV is initiated. For the preterm infant, oxygen should be blended to goal saturation targets. In summary: (1) Use room air in the baby is cyanotic or needs PPV. (2) If the baby is less than 32 weeks, titrate oxygen ( Table 79.3 ). (3) Use 100% oxygen if chest compressions or medications are given, then titrate to targeted SpO 2 . (4) Apply oximeter to right hand (preductal).
Time after Birth (min) | Target SpO 2 (%) |
---|---|
1 | 60-65 |
2 | 65-70 |
3 | 70-75 |
4 | 75-80 |
5 | 80-85 |
10 | 85-95 |
Breathing usually begins by 30 seconds after birth and is sustained by 90 seconds of age. A few minutes after birth, the respiratory rate (RR) of normal neonates is between 40 and 60 breaths/min. The absence of a pause between inspiration and expiration helps develop and maintain functional residual capacity (FRC). Apnea and bradypnea prolong exhalation, reduce FRC, and cause hypoxia. Causes of apnea and bradypnea include severe acidosis, asphyxia, maternal drugs, infections, and CNS damage. Tachypnea (>60 breaths/min) occurs with hypoxemia, hypovolemia, metabolic and respiratory acidosis, CNS hemorrhage, pulmonary gas leaks, pulmonary disease (e.g., hyaline membrane disease, aspiration syndromes, infections), pulmonary edema, and maternal drugs (e.g., narcotics, alcohol, magnesium, barbiturates).
Recommendations now are that initial breaths should be at 20 cm H 2 O. Ventilation should be performed at 40 to 60 breaths/min with reassessment of HR, color, and breath sounds. In the neonate, rising HR may be the best assessment of adequate ventilation. If gastric distention becomes a problem, hindering compliance, a gastric tube may be placed (8 Fr) to improve compliance. Both sides of the chest should rise equally and simultaneously with inspiration, but the amount of rise should not exceed that associated with the neonate’s normal spontaneous breathing. The presence of breath sounds may be misleading because they are well transmitted within the neonate’s small chest. A difference in breath sounds between the two sides of the chest should raise suspicion of endobronchial intubation, pneumothorax, atelectasis, or a congenital anomaly of the lung. The presence of loud breath sounds over the stomach suggests esophageal intubation or a tracheoesophageal fistula. If ventilation is adequate, the neonate will become pink, initiate rhythmic breathing, and have a normal HR.
Because most asphyxiated neonates have no lung disease, they can be effectively ventilated with peak airway pressures lower than 25 cm H 2 O, even for the first few breaths. Those with stiff lungs (e.g., erythroblastosis fetalis, congenital anomalies of the lung, pulmonary edema, severe meconium aspiration, diaphragmatic hernia) may require higher inspiratory pressure to ventilate their lungs and are more likely to have pulmonary gas leaks. To reduce this likelihood, the lungs should first be ventilated with an inspiratory pressure of 15 to 20 cm H 2 O and inspiratory rate of 150 to 200 breaths/min. If low-pressure (low-volume), high-rate ventilation does not improve the oxygenation, higher pressure and volume may be required. Failure to adequately ventilate the lungs at birth may worsen hypoxemia and lead to CNS damage or even death. If P a O 2 exceeds 70 to 80 mm Hg or SaO 2 exceeds 94%, the inspired oxygen concentration should be reduced (if increased concentrations of oxygen are used) until SaO 2 and PaO 2 are normal for age. Oxygenation is maintained at the low range of normal in neonates 34 weeks’ or less gestation to avoid the retinopathy of prematurity. The neonate’s HR should be monitored continuously during endotracheal intubation because the process of tracheal intubation may cause arrhythmias in hypoxic neonates.
If the practitioner is having difficulty with bag mask ventilation or fails intubation, a laryngeal mask airway (LMA) should be considered.
Pneumothorax occurs in 1% of all vaginal deliveries, in 10% of meconium-stained neonates, and in 2% to 3% of neonates who require mechanical ventilation in the delivery room. The hemithorax containing free air is usually hyperexpanded and moves poorly with ventilation. The point of maximum cardiac impulse is shifted toward the side without the pneumothorax. Heart tones may be muffled.
If a small, high-intensity cold light is placed directly on the skin of the neonate’s chest, the involved side of the chest will glow if a pneumothorax is present. Pneumothoraces are relieved by needle or chest tube drainage.
The head should be placed in a neutral or “sniffing” position during bag-and-mask ventilation and tracheal intubation. An appropriately sized endotracheal tube (ETT) is inserted and its tip is placed 1 to 2 cm below the vocal cords, depending on the size of the neonate. Usually, this means that the distance from the tip of the tube to the gums is 7, 8, 9, or 10 cm in 1-, 2-, 3-, and 4-kg infants. A small gas leak should be present between the ETT and trachea when the ventilation pressure is 15 to 25 cm H 2 O. This usually entails the use of a 2.5-mm (internal diameter) tube for neonates weighing less than 1.5 kg, a 3.0-mm tube for those between 1.5 and 2.5 kg, and a 3.5-mm tube for those weighing more than 2.5 kg. Successful tracheal intubation is confirmed by observing the ETT pass through the vocal cords, by observing bilateral chest movement with each mechanical inspiration, and by observing condensation in the ETT during exhalation. Breath sounds should be much louder over the chest than over the abdomen, and the skin color, HR, and SaO 2 should improve with positive-pressure ventilation. Carbon dioxide should be present during exhalation. However, the small tidal volumes and low pulmonary blood flow of some infants at birth may make it difficult to use capnography effectively.
Place both thumbs on the sternum and allow the fingers to support the back ( Fig. 79.3 ). Compress the sternum to approximately one-third the depth of the chest. Three compressions should be performed with a breath in place of the fourth compression for an effective compression rate of 90 compressions and 30 breaths/min. HR should be evaluated every 45 to 60 seconds, and if after adequate ventilation and compressions for 60 seconds the HR is still less than 60 beats/min, then medications should be considered.
Resuscitation with medications are needed only for the infant that is critically depressed or presents with significant anomalies leading to cardiovascular depression. There should be a quick reference drug list designed for each delivery room for easy access for these rare occasions, and should help with dosing based on an estimated weight of the infant at birth. IV route of administration is the preferred for administration of resuscitation medications; however, IO and umbilical venous catheters can be placed rapidly by trained individuals and may be life-saving.
The primary medication used in the resuscitation of a newborn is epinephrine, and should be given if the infant’s HR is less than 60 bpm, 45 to 60 seconds after the initiation of PPV and chest compressions. The recommended dose is 0.1 to 0.3 mL/kg of 1:10,000 concentration; (0.01-0.03 mg/kg), followed by a 1 mL flush of saline. While IV administration is preferable, if venous access is not obtained, it is appropriate to give epinephrine via the ETT. In this instances the practitioner, should give a higher dose of Epinephrine: 0.5 to 1 mL/kg of 1:10,000 concentration; (0.05-0.1 mg/kg). Epinephrine can be repeated every five minutes, as needed, while re-evaluating HR every 45 to 60 seconds.
Naloxone (Narcan) is not recommended as an initial response to respiratory distress in neonatal resuscitation. Neonates should be supported on PPV, even in women who have received narcotics less than four hours prior to delivery. However, if respiratory depression continues, naloxone can be considered. In addition, naloxone should be avoided in an infant whose mother has a history of narcotic dependence due to the risk of seizures from withdrawal.
Hypovolemia is detected by measuring arterial blood pressure and by physical examination (i.e., skin color, perfusion, capillary refill time, pulse volume, and extremity temperature).
CVP measurements are useful in detecting hypovolemia and in determining the adequacy of fluid replacement. The venous pressure of normal neonates is 2 to 8 cm H 2 O. If CVP is less than 2 cm H 2 O, hypovolemia should be suspected.
Treatment of hypovolemia requires expansion of intravascular volume with blood and crystalloid. Albumin may also be used, but evidence of its effectiveness is limited. If it is suspected that the neonate will be hypovolemic at birth, Rh-negative type O packed RBCs should be available in the delivery room before the neonate is born. Crystalloid and blood should be titrated in 10 mL/kg and given slowly over 10 minutes, if hemodynamics allow, to limit the risk of intraventricular hemorrhage.
Occasionally, enormous volumes of blood and fluid are required to raise arterial blood pressure to normal. At times, more than 50% of the blood volume (85 mL/kg in term neonates and 100 mL/kg in preterm neonates) must be replaced, especially when the placenta is transected or abrupted during birth. In most cases, less than 10 to 20 mL/kg of volume restores mean arterial pressure to normal.
Hypoglycemia, hypocalcemia, and hypermagnesemia also cause hypotension in neonates. Hypotension induced by alcohol or magnesium intoxication usually responds to blood volume expansion or dopamine, or to both. Hypermagnesemic neonates generally respond to 100 to 200 mg/kg of calcium gluconate administered over a 5-minute period.
Meconium stained amniotic fluid (MSAF) when aspirated into the lungs during delivery or in utero can cause serious lung injury and respiratory distress syndrome (RDS). Most cases of meconium aspiration occur in utero; therefore, endotracheal intubation to suction the airway to remove MSAF should only occur if the neonate is distress: absent or depressed respirations, HR less than 100 bpm, or poor muscle tone. A depressed MSAF stained infant should be intubated as soon as possible following delivery. Suctioning is accomplished through an ETT, and if there is a significant amount of MSAF or the infant remains in extremis, they should be transferred directly to the neonatal ICU.
Essentially all neonates have a blue-tinged cast to their skin at birth. By 60 seconds of age, most of them are entirely pink, except for their hands and feet, which remain blue. If central cyanosis persists beyond 90 seconds of age, asphyxia, low cardiac output, pulmonary edema, methemoglobinemia, polycythemia, congenital heart disease, arrhythmias, and pulmonary disorders (e.g., respiratory distress, airway obstruction, hypoplastic lungs, diaphragmatic hernia) should be considered, especially if the infant remains cyanotic despite oxygen and controlled ventilation. Neonates who are pale at birth are often asphyxiated, hypovolemic, acidotic, or anemic, or they have congenital heart disease. A neonate whose skin is entirely pink within 2 minutes of birth may be intoxicated with alcohol or magnesium or may be alkalotic (pH >7.50). Rubrous neonates are usually polycythemic.
Resuscitation beds should allow positioning of the neonate’s head below the level of the lungs to promote drainage of lung fluid and reduce the likelihood of aspirating gastric contents. A servo-controlled infrared heater should be used to maintain the neonate’s temperature between 36°C and 37°C, unless there is evidence of asphyxia. If asphyxia is noted, body temperature should be reduced to 34°C to 35°C for brain protection. A suction device should be available and should allow the suction pressure to be varied; pressures below −100 mm Hg should not be used.
Equipment required for tracheal intubation includes 0 and 00 straight laryngoscope blades; a pencil-type laryngoscope handle; 2.5-, 3.0-, and 3.5-mm ETTs; and a suction catheter that easily fits through each size tube. The ventilation system must permit ventilatory rates of at least 150 breaths/min and make it possible to maintain positive end expiratory pressure (PEEP). One-way valves can stick in the closed position, especially when high gas flow and high RRs are used. The modified Jackson-Rees or Ayres system works well when appropriately trained people use it. Overexpansion of the lungs with large tidal volumes injures the lungs and activates inflammatory processes that may cause chronic lung disease. Gentle inflation of the lung is less injurious to the lung. Airway inflation pressures should be measured continuously during assisted or controlled ventilation in the delivery room, and excessive pressures and tidal volumes should be avoided. As in any critical care situation, patient care should be guided by information. Consequently, blood gas and pH measurements are mandatory, and the results of these tests must be available within 10 minutes of drawing the blood sample. Umbilical arterial catheters are useful for measuring arterial blood pressure and withdrawing blood for blood gas analysis and pHa. They can also be used to infuse emergency fluids. Arterial oxygen saturation (SaO 2 ) can be measured immediately after birth by attaching a pulse oximeter to a hand or foot. Pulse oximeters permit rapid detection of changes in oxygenation and rapid reduction of fraction of inspired oxygen (FiO 2 ). The normal SaO 2 of neonates is usually 87% to 95%, which is associated with a PaO 2 of 55 to 70 mm Hg.
Pediatric cardiac arrest is not a rare event. At least 16,000 American children (8-20/100,000 children/year) suffer a cardiopulmonary arrest each year. More than half of these cardiac arrests probably occur in-hospital. With advances in resuscitation science and implementation techniques, survival from pediatric cardiac arrest has improved substantially over the past 25 years.
Outcomes from pediatric cardiac arrest have improved significantly over the past 20 years. For example, survival to discharge from pediatric in-hospital cardiac arrest has increased from less than 10% in the 1980s to greater than 25% in the 21st century. Of the pediatric patients that survive to hospital discharge, nearly three quarters will have favorable neurologic function defined by specific pediatric cerebral outcome measures and quality of life indicators. Factors that influence outcome from pediatric cardiac arrest include (1) the pre-existing condition of the child; (2) the environment in which the arrest occurs; (3) the initial ECG rhythm detected; (4) the duration of no-flow time (the time during an arrest without spontaneous circulation or CPR); (5) the quality of the life-supporting therapies provided during the resuscitation; and (6) the quality of the life-supporting therapies during postresuscitation.
Not surprisingly, outcomes after pediatric out-of-hospital arrests are much worse than those after in-hospital arrests. This may be due to the fact that there is a prolonged period of no flow in out-of-hospital arrests, where many of the pediatric cardiac arrests are not witnessed and only 30% of children are provided with bystander CPR. As a result of these factors, less than 10% of cases of pediatric out-of-hospital cardiac arrest (OHCA) survive to hospital discharge, and for those that do survive, severe neurological injury is common. These findings are especially troublesome, given that bystander CPR more than doubles patient survival rates in adults. An exciting prospective, nationwide, population-based cohort study from Japan similarly demonstrates more than doubling of survival rates for children who have OHCA and receive bystander CPR either with conventional CPR (with rescue breathing) or chest compression only CPR compared with no bystander CPR. The same study then further stratifies outcomes for OHCA into “cardiac” and “noncardiac” causes for arrest, and defines the relative value of rescue breathing during CPR by bystanders. Pediatric patients who have OHCA with noncardiac causes and receive bystander conventional CPR (including rescue breathing) had an association with higher frequency of favorable neurologic outcomes at 1 month after arrest compared with compression-only bystander CPR or no bystander CPR. For pediatric arrests defined as “cardiac” in nature, bystander CPR (conventional or compression-only) was associated with a higher rate of favorable neurologic outcomes 1 month after arrest compared with no bystander CPR. Interestingly, the two types of bystander CPR (conventional or compression-only) seemed to be similarly effective for pediatric cardiac arrests with cardiac causes, consistent with animal and adult studies.
Survival outcomes after in-hospital cardiac arrest are higher in the pediatric population compared with adults; 27% of children survive to hospital discharge compared with only 17% of adults. For both children and adults, outcomes are better after arrhythmogenic arrests, ventricular fibrillation (VF)/ventricular tachycardia (VT). Importantly, pediatric in-hospital arrests are less commonly caused by arrhythmias (10% of pediatric arrests vs. 25% of adult arrests), and approximately one-third of children and adults with these arrhythmogenic arrests survive to hospital discharge. Interestingly, the superior pediatric survival rate following in-hospital cardiac arrest reflects a substantially higher survival rate among children with asystole or pulseless electrical activity (PEA) compared with adults (24% vs. 11%). Further investigations have shown that the superior survival rate seen in children is mostly attributable to a much better survival rate among infants and preschool age children compared with older children. Although speculative, the higher survival rates in children may be due to improved coronary and cerebral blood flow (CBF) during CPR because of increased chest compliance in these younger arrest victims, with improved aortic diastolic pressure and venous return. In addition, survival of pediatric patients from an in-hospital cardiac arrest is more likely in hospitals staffed with dedicated pediatric physicians.
The four distinct phases of cardiac arrest and CPR interventions are (1) prearrest, (2) no flow (untreated cardiac arrest), (3) low flow (CPR), and (4) postresuscitation/arrest. Interventions to improve outcome of pediatric cardiac arrest should optimize therapies targeted to the time and phase of CPR, as suggested in Table 79.4 .
Phase | Interventions |
---|---|
Prearrest phase (protect) | Optimize patient monitoring and rapid emergency response Recognize and treat respiratory failure or shock to prevent cardiac arrest |
Arrest (no-flow) phase (preserve) | Minimize interval to BLS and ACLS Organize response with clear leadership Minimize interval to defibrillation, when indicated |
Low-flow (CPR) phase (resuscitate) | Push hard, push fast Allow full chest recoil Minimized interruptions in compressions Avoid overventilation Titrate CPR to optimize myocardial blood flow (coronary perfusion pressures and exhaled CO 2 ) Consider adjuncts to improve vital organ perfusion during CPR Consider ECMO if standard CPR/ALS not promptly successful |
Post-resuscitation phase: short-term | Optimize cardiac output and cerebral blood flow Treat arrhythmias, if indicated Avoid hyperglycemia, hyperthermia, hyperventilation Debrief to improve future responses to emergencies |
Postresuscitation phase: long-term rehabilitation (regenerate) | Early intervention with occupational and physical therapy Bioengineering and technology interface Possible future role for stem cell transplantation |
The prearrest phase refers to any relevant preexisting conditions of the child (e.g., neurologic, cardiac, respiratory, or metabolic problems) and precipitating events (e.g., respiratory failure or shock), uncoupling metabolic delivery and metabolic demand. Pediatric patients who suffer an in-hospital cardiac arrest often have changes in their physiological status in the hours leading up to their arrest event. Therefore, interventions during the prearrest phase focus on preventing the cardiac arrest, with special attention to early recognition and targeted treatment of respiratory failure and shock. Early recognition plays a key role in identifying a prearrest state in children, who unlike adults may be able to mount a prolonged physiologic response to a worsening clinical picture. Medical emergency teams (METs; also known as rapid response teams ) are in-hospital emergency teams designed specifically for this purpose. Front-line providers, and even parents, are encouraged to initiate evaluation by METs based on physiologic protocol driven parameters or even intuition. Patients are assessed by the METs, and those at high risk of clinical decompensation are transferred to a pediatric ICU if necessary, with the goal to prevent progression to full cardiac arrest or to decrease the response time to initiation of advanced life support, thereby limiting the no-flow state. Implementation of METs decreases the frequency of cardiac arrests compared with retrospective control periods before MET initiation. While early recognition protocols cannot identify all children at risk for cardiac arrest, it seems reasonable to assume that transferring critically ill children to an ICU early in their disease process for better monitoring and more aggressive interventions can improve resuscitative care and clinical outcomes. The caveat is that prearrest states must be identified to initiate monitoring and interventions that may inhibit the progression to an arrest. While a significant amount of research dollars and resources are spent on the other phases of cardiac arrest, particular focus on the prearrest state may yield the greatest improvement in survival and neurologic outcomes.
For OHCA victims, “compression-only” CPR has been associated with improved outcomes. This is now the recommended modality for emergency medical service dispatcher instructing bystander CPR. In a recent Japanese study, children with OHCA due to a primary cardiac etiology displayed an equivalent survival rate between compression-only CPR and classic CPR with rescue breaths. However, only 29% of patients had a cardiac cause of OHCA. Those with noncardiac etiology in the overall cohort had a significantly worse survival rate with compression-only CPR, as compared with classic CPR with rescue breaths. Additionally, in another nationwide Japanese OHCA registry study, compression-only CPR was superior to no bystander CPR at all but not to conventional CPR. In a recent American OHCA registry study, children who received conventional bystander CPR with chest compressions and rescue breaths had improved rates of overall survival and survival with favorable outcomes as compared with those who did not receive CPR, whereas those receiving compression-only CPR did not fare any better than children not receiving CPR. Thus compression-only CPR is not recommended for children in either the inpatient or out-of-hospital setting, except in situations in which “rescuers are unwilling or unable to deliver breaths.”
Regardless, the prioritization of initial interventions during CPR has shifted from airway-breathing-circulation (“A-B-C”) to circulation-airway-breathing (“C-A-B”) in order to prevent harmful delays in the initiation of chest compressions and due to the relative complexity of the tasks involved in providing assisted ventilation. This is endorsed by both the 2010 and 2015 AHA BLS Guidelines. However, a 2015 International Liaison Committee on Resuscitation consensus statement identified a paucity of pediatric-specific evidence to support this recommendation. In our opinion, the approach is physiologically sound, especially given the association of delayed chest compression initiation with poor outcomes. With that said, the pediatric provider must consider the predominance of asphyxia and hypoxemia as precursors to cardiac arrest. This is especially true in the ICU and operating room, where personnel and other resources frequently allow for simultaneous circulatory support with high-quality chest compressions as well as the provision of assisted ventilations by experienced personnel.
In order to improve outcomes from pediatric cardiac arrest, it is imperative to shorten the no-flow phase of untreated cardiac arrest. To that end, it is important to monitor high-risk patients to allow early recognition of the cardiac arrest and prompt initiation of basic and advanced life support. Effective CPR optimizes coronary perfusion pressure (by elevating aortic diastolic pressure relative to RAP) and cardiac output to critical organs to support vital organ viability (by elevating mean aortic pressure) during the low flow phase. Important tenets of basic life support are push hard, push fast, allow full chest recoil between compressions, and minimize interruptions of chest compression . The myocardium receives blood flow from the aortic root, mainly during diastole, via the coronary arteries. When the heart arrests and no blood flows through the aorta, coronary blood flow ceases. However, during chest compressions, aortic pressure rises at the same time as RAP and with the subsequent decompression phase of chest compressions, the RAP falls faster and lower than the aortic pressure, which generates a pressure gradient that perfuses the heart with oxygenated blood. Therefore, full elastic recoil (release) is critical to create a pressure difference between the aortic root and the right atrium. A CPP below 15 mm Hg during CPR is a poor prognostic factor for ROSC. Achieving optimal coronary perfusion pressure, exhaled carbon dioxide concentration, and cardiac output during the low flow phase of CPR is consistently associated with an improved chance for return of spontaneous circulation (ROSC) and improved short- and long-term outcome in mature animal and human studies. There is a critical need for research evaluating goal directed CPR, both in immature animal models and pediatric patients. Other measures essential for truncating the no-flow phase during VF and pulseless VT are rapid detection and prompt defibrillation. Clearly, CPR alone is inadequate for successful resuscitation from these arrhythmias. For cardiac arrests resulting from asphyxia and/or ischemia, provision of adequate myocardial perfusion and myocardial oxygen delivery are the critical elements for ROSC.
The postarrest/resuscitation phase includes coordinated, skilled management of the immediate post-resuscitation stage, the next few hours to days, and long-term rehabilitation. The immediate post-resuscitation stage is a high-risk period for ventricular arrhythmias and other reperfusion injuries. Goals of interventions implemented during the immediate post-resuscitation stage and the next few days include adequate tissue oxygen delivery, treatment of post-resuscitation myocardial dysfunction, and minimizing post-resuscitation tissue injury (e.g., preventing post-resuscitation hyperthermia and hypoglycemia; and, perhaps initiating post-resuscitation therapeutic hypothermia, preventing hyperglycemia and avoiding hyperoxia). This post-arrest/resuscitation phase may have the greatest potential for innovative advances in the understanding of cell injury (excitotoxicity, oxidative stress, metabolic stress) and cell death (apoptosis and necrosis), ultimately leading to novel molecular-targeted interventions. The rehabilitation stage concentrates on salvage of injured cells, and support for reengineering of reflex and voluntary communications of these cell and organ systems to improve long-term functional outcome.
The specific phase of resuscitation dictates the focus of care. Interventions that improve outcome during one phase may be deleterious during another. For instance, intense vasoconstriction during the low flow phase of cardiac arrest improves coronary perfusion pressure and the probability of ROSC. The same intense vasoconstriction during the post-resuscitation phase increases left ventricular afterload and may worsen myocardial strain and dysfunction. Current understanding of the physiology of cardiac arrest and recovery allows us to only crudely manipulate blood pressure, oxygen delivery and consumption, body temperature, and other physiologic parameters in our attempts to optimize outcome. Future strategies likely will take advantage of increasing knowledge of cellular injury, thrombosis, reperfusion, mediator cascades, cellular markers of injury and recovery, and transplantation technology, including stem cells.
During CPR, cardiac output and pulmonary blood flow are ∼10% to 25% of that during normal sinus rhythm; therefore, a lower minute ventilation is necessary for adequate gas exchange from the blood traversing the pulmonary circulation. Animal and adult data indicate that overventilation (“overventilation” from exuberant rescue breathing) during CPR is common and can substantially compromise venous return and subsequently cardiac output. These detrimental hemodynamic effects are compounded when one considers the effect of interruptions in CPR to provide airway management and rescue breathing and may contribute to worse survival outcomes. While overventilation is problematic, in light of the fact that most pediatric arrests are asphyxial in nature, immediate initiation of adequate ventilation is still important. The difference between arrhythmogenic and asphyxial arrests lies in the physiology. In animal models of sudden VF cardiac arrest, acceptable PaO 2 and PaCO 2 persist for 4 to 8 minutes during chest compressions without rescue breathing. This is in part because aortic oxygen and carbon dioxide concentrations at the onset of the arrest do not vary much from the prearrest state with no blood flow and minimal aortic oxygen consumption. The lungs act as a reservoir of oxygen during the low-flow state of CPR; therefore, adequate oxygenation and ventilation can continue without rescue breathing. Several retrospective studies of witnessed VF cardiac arrest in adults have also shown that outcomes are similar after bystander-initiated CPR with either chest compressions alone or chest compressions plus rescue breathing. However, during asphyxial arrest, peripheral and pulmonary blood flow continues during the prearrest, state resulting in significant arterial and venous oxygen desaturation, elevated lactate levels, and depletion of the pulmonary oxygen reserve. Therefore, at the onset of CPR, there is substantial arterial hypoxemia and resulting acidemia. In this circumstance, rescue breathing with controlled ventilation can be a life-saving maneuver. In contrast, the adverse hemodynamic effects from overventilation during CPR combined with possible interruptions in chest compressions to open the airway and deliver rescue breathing are a lethal combination in certain circumstances such as VT/VF arrests. In short, the resuscitation technique should be titrated to the physiology of the patient to optimize patient outcome.
When the heart arrests, no blood flows to the aorta and coronary blood flow ceases immediately. At that point, provision of high quality CPR (PUSH HARD, PUSH FAST) is vital to reestablish coronary flow. The goal during CPR is to maximize the myocardial perfusion pressure (MPP). Related by the following equation: MPP = aortic diastolic blood pressure (AoDP) minus RAP, myocardial blood flow improves as the gradient between AoDP and RAP increases. During downward compression phase, aortic pressure rises at the same time as RAP with little change in the MPP. However, during the decompression phase of chest compressions, the RAP falls faster and lower than the aortic pressure, which generates a pressure gradient perfusing the heart with oxygenated blood during this artificial period of “diastole.” Several animal and human studies have demonstrated, in both VT/VF and asphyxial models, the importance of establishing MPP as a predictor for short-term survival outcome (ROSC). Because there is no flow without chest compressions, it is important to minimize interruptions in chest compressions. To allow good venous return in the decompression phase of external cardiac massage, it is also important to allow full chest recoil and to avoid overventilation (preventing adequate venous return because of increased intrathoracic pressure).
Based on the provided equation, MPP can be improved by strategies that increase the pressure gradient between the aorta and the right atrium. As an example, the inspiratory impedance threshold device (ITD) is a small, disposable valve that can be connected directly to the tracheal tube or face mask to augment negative intrathoracic pressure during the inspiratory phase of spontaneous breathing and the decompression phase of CPR by impeding airflow into the lungs. Application in animal and adult human trials of CPR has established the ability of the ITD to improve vital organ perfusion pressures and myocardial blood flow ; however, in the only randomized trial during adult CPR, mortality benefit was limited to the subgroup of patients with PEA. Additional evidence that augmentation of negative intrathoracic pressure can improve perfusion pressures during CPR comes from the active compression-decompression device (ACD). The ACD is a handheld device that is fixed to the anterior chest of the victim by means of suction similar to a household plunger that can be used to apply active decompression forces during the release phase, thereby creating a vacuum within the thorax. By actively pulling during the decompression phase, blood is drawn back into the heart by the negative pressure. Animal and adult studies have demonstrated that the combination of ACD with ITD act in concert to further improve perfusion pressures during CPR compared with ACD alone. In the end, while novel interventions such as the ITD and ACD are promising adjuncts to improve blood flow during CPR, the basic tenants of PUSH HARD, PUSH FAST, ALLOW FULL CHEST WALL RELEASE, MINIMIZE INTERRUPTIONS, and DON’T OVERVENTILATE are still the dominate factors to improve blood flow during CPR and chance of survival.
The pediatric chest compression depth recommendation of at least one-third anterior-posterior chest depth (approximately 4 cm in infants and 5 cm in children) is based largely upon expert clinical consensus, using data extrapolated from animal, adult, and limited pediatric data. In a small study of six infants, chest compressions targeted to one half anterior-posterior chest depth resulted in improved systolic blood pressures, compared with those targeted at one-third anterior-posterior chest depth. While only a small series with qualitatively estimated chest compression depths, this is the first study to collect actual data from children supporting the existing chest compression depth guidelines. On the contrary, two recent studies using computer automated tomography (CT) suggest that depth recommendations based on a relative (%) anterior-posterior chest compression depth are deeper than that recommended for adults, and that a depth of one half anterior-posterior chest depth will result in direct compression to the point of fully emptying the heart and requisite shifting of heart because of inadequate AP diameter reserve in most children. Future studies that collect data from actual children and that associate quantitatively measured chest compression depths with short- and long-term clinical outcomes (arterial blood pressure, end tidal carbon dioxide, ROSC, survival) are needed.
The amount of ventilation provided during CPR should match, but not exceed, perfusion and should be titrated to the amount of circulation during the specific phase of resuscitation, as well as the metabolic demand of the tissues. Therefore, during the low flow state of CPR when the amount of cardiac output is roughly 10% to 25% of normal, less ventilation is needed. However, the best ratio of compressions to ventilations in pediatric patients is largely unknown and depends on many factors, including the compression rate, the tidal volume, the blood flow generated by compressions, and the time that compressions are interrupted to perform ventilation. Recent evidence demonstrates that a compression/ventilation ratio of 15:2 delivers the same minute ventilation and increases the number of delivered chest compressions by 48% compared with CPR at a compression/ventilation ratio of 5:1 in a simulated pediatric arrest model. This is important because when chest compressions cease, the aortic pressure rapidly decreases and coronary perfusion pressure falls precipitously, thereby decreasing myocardial oxygen delivery. Increasing the ratio of compressions to ventilations minimizes these interruptions, thus increasing coronary blood flow. The benefits of PPV (increased arterial content of oxygen and carbon dioxide elimination) must be balanced against the adverse consequence of decreased circulation. These findings are in part the reason the AHA now recommends a pediatric compression/ventilation ratio of 15:2 .
In a model of human adult cardiac arrest, cardiac output and coronary blood flow are optimized when chest compressions last for 30% of the total cycle time (approximately 1:2 ratio of time in compression to time in relaxation). As the duration of CPR increases, the optimal duty cycle may increase to 50%. In a juvenile swine model, a relaxation period of 250 to 300 milliseconds (duty cycle of 40%-50% at a compression rate of 120/min) correlates with improved cerebral perfusion pressures (CPPs) compared with shorter duty cycles of 30%.
In adult and animal models of cardiac arrest, circumferential (vest) CPR has been demonstrated to dramatically improve CPR hemodynamics. In smaller infants, it is often possible to encircle the chest with both hands and depress the sternum with the thumbs, while compressing the thorax circumferentially (thoracic squeeze). In an infant animal model of CPR, this “two-thumb” method of compression with thoracic squeeze resulted in higher systolic and diastolic blood pressures and a higher pulse pressure than traditional two-finger compression of the sternum. Although not rigorously studied, our clinical experience indicates that it is very difficult to attain adequate chest compression force and adequate aortic pressures with the two-finger technique, so we fully support the AHA Guidelines for health care providers to perform CPR on infants with the two-thumb-encircling hands technique.
In animal models, high quality standard, closed-chest CPR generates myocardial blood flow that is greater than 50% of normal, CBF that is approximately 50% of normal, and cardiac output ∼10% to 25% of normal. By contrast, open-chest CPR can generate myocardial and CBF that approaches normal. Although open-chest massage improves coronary perfusion pressure and increases the chance of successful defibrillation in animals and humans, performing a thoracotomy to allow open-chest CPR is impractical in many situations. A retrospective review of 27 cases of CPR following pediatric blunt trauma (15 with open-chest CPR and 12 with closed-chest CPR) demonstrated that open-chest CPR increased hospital cost without altering rates of ROSC or survival to discharge. However, survival in both groups was 0%, indicating that the population may have been too severely injured or too late in the process to benefit from this aggressive therapy. Open-chest CPR is often provided to children after open-heart cardiac surgery and sternotomy. Earlier institution of open-chest CPR may warrant reconsideration in selected special resuscitation circumstances.
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