Crit Care Nurse 2008 Feb; 28(1): 42-63
Pediatric Care
CE Article
Viral Myocarditis in Children
Tammy L. Uhl, RN, MSN, CCRN, CCNS
Tammy L. Uhl is a pediatric critical care clinical nurse specialist at Brenner Children’s Hospital, Wake Forest University Baptist Medical Center, Winston-Salem, North Carolina.
To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899–1712 or (949) 362–2050 (ext 532); fax, (949) 362–2049; e-mail, reprints{at}aacn.org.
Financial Disclosures
None reported.
This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:- Identify which population is at most risk of death as the result of myocarditis
- Identify the mechanism that results in morbidity and mortality in children with myocarditis
- Discuss the signs and symptoms of myocarditits in children
- Describe the treatment of patients with myocarditis
Corresponding author: Tammy L. Uhl, RN, MSN, CCRN, CCNS, Brenner Children’s Hospital, Wake Forest University Baptist Medical Center, Medical Center Blvd, Winston-Salem, NC 27157 (e-mail: tuhl{at}wfubmc.edu).
Myocarditis is defined as inflammation of the myocardium followed by necrosis and/or degeneration of myocytes.1–3 The inflammation can be diffuse or focal and is usually due to an infection.
Although myocarditis severe enough to be recognized is rare, it is the most common cause of heart failure in otherwise healthy children.4 In both children and adults, most cases are subclinical; thus, the true incidence of myocarditis in children is unknown.2,5–7 Unfortunately, the clinical features of myocarditis can vary widely, and often no cardiac signs or symptoms occur, complicating recognition. For children in whom the diagnosis is suspected or cardiovascular compromise is severe enough to require admission to the pediatric intensive care unit (PICU), critical care nurses are an essential component in determining management, care, and outcomes. In this article, I describe the etiology of viral myocarditis in children, potential insidious clinical features, pathophysiology of the disease, and critical care management.
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Case 1
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A.J., a previously healthy 3-year-old boy, was brought to the emergency department because his body temperature was 40.5°C. During the previous week, he had had some nasal discharge and a mild, nonproductive cough. He had no history of increased work of breathing, rashes, or diarrhea. One day before the visit to the emergency department, he had been vomiting and had been unable to tolerate anything by mouth.
On arrival in the emergency department, A.J. appeared ill but was alert and in no marked distress. Vital signs were heart rate, 162/min; respirations, 26/min; and oxygen saturation, determined by pulse oximetry, 99% on room air. No murmur or gallop was noted; capillary refill was brisk with 2+ peripheral pulses and warm extremities. Breath sounds were clear bilaterally. He appeared mildly dehydrated with tachycardia, mildly sunken eyes, and tacky mucous membranes.
Routine blood tests were done. Electrolyte levels were normal except for a carbon dioxide level of 18 mEq/L, an anion gap of 23 mEq/L, and a serum urea nitrogen level of 21 mg/dL (to convert to millimoles per liter, multiply by 0.357), consistent with dehydration. A complete blood cell count revealed a white blood cell count of 26900/µL, a hemoglobin level of 12 g/dL, a hematocrit of 35.9%, and a platelet count of 321000/µL. A differential count was not completed.
Approximately 15 minutes after his initial examination, A.J. received two 20 mL/kg intravenous boluses of normal saline and was given something to eat, which he tolerated well. Because his parents were comfortable with observing the child at home and expressed full understanding of the signs of dehydration, A.J. was readied for discharge.
While the discharge papers were being completed, A.J. suddenly became unresponsive and apneic. Bag-valve -mask ventilation was begun, and subsequently he was pulseless. Cardiopulmonary resuscitation was initiated. After a prolonged attempt at resuscitation, he was pronounced dead. Postmortem examination revealed myocarditis of probable viral origin.
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Case 2
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K.M., a 5-year-old boy with a history of asthma, was brought to the emergency department because he had fainted. After the syncopal episode, he had shortness of breath and tachypnea. Approximately 4 days before this visit to the emergency department, he had had gastroenteritis with vomiting and diarrhea that resolved. Findings on a physical examination were unremarkable except for bilateral wheezing and increased work of breathing. He was given several albuterol nebulizers for a suspected exacerbation of asthma. A chest radiograph revealed bilateral infiltrates thought to be consistent with Mycoplasma pneumonia. He was given azithromycin and was transferred to a tertiary care center for closer observation.
On arrival in the PICU, his respiratory status continued to deteriorate. He was markedly tachypneic. Oxygen saturations were 86% to 91% on a 100% nonrebreather mask. Continuous albuterol was begun, but his pulmonary status did not change. Auscultation revealed diminished breath sounds at the bases bilaterally, no wheezing, and no murmur but a gallop. A repeat chest radiograph revealed pulmonary edema and cardiomegaly. After the repeat radiograph and continuing respiratory deterioration, he was intubated and mechanical ventilation was started. Within minutes of intubation, clinically significant unifocal premature ventricular contractions and hypotension (50–60/20–30 mm Hg) developed. He was given a lidocaine bolus, and continuous infusions of both lidocaine and epinephrine were started. Laboratory studies revealed a white blood cell count of 7300/µL, a hemoglobin level of 11.1 g/dL, a platelet count of 103000/µL, and unremarkable electrolyte levels. An echocardiogram showed markedly decreased left ventricular function with an ejection fraction of 10% to 14% and diminished right ventricular function. Neither structural abnormalities nor pericardial effusion was seen. A 12-lead electrocardiogram showed a normal sinus rhythm with frequent premature ventricular contractions and nonspecific T-wave abnormalities (Figure 1
). The diagnosis was acute myocarditis with severe cardiomyopathy. Because of the continued deterioration in K.M.’s condition, inability to oxygenate, and worsening cardiac function, extracorporeal membrane oxygenation (ECMO) was started.
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Figure 1 K.M.’s electrocardiogram on admission to the pediatric intensive care unit shows sinus tachycardia, frequent unifocal premature ventricular contractions, and nonspecific T-wave abnormality.
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ECMO was discontinued on hospital day 13. K.M. made steady improvement, although he continued to require vasoactive support and mechanical ventilation for another 6 days. He was extubated on hospital day 19. At that time, his ejection fraction was approximately 35%. He was subsequently transferred to the pediatric rehabilitation unit, from which he eventually was discharged to home; the diagnosis was severe dilated cardiomyopathy.
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Incidence and Prevalence
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Myocarditis appears to be more common in children than in adults.8 Its true incidence, however, is unknown; it is thought that subclinical cases ("silent" myocarditis) occur much more often than do severe cases. Many cases are unrecognized because of the wide range of signs and symptoms and, in some patients, the complete lack of clinical findings.8,9 In a postmortem study of children who died without a history suggestive of myocarditis, researchers found evidence of active or healed myocarditis in 17 of 138 cases (12.3%).8,10 Of the 17 cases, 15 occurred in children who died suddenly. In postmortem studies in adults, myocardial inflammation occurred in 1% to 9%.8
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Etiology
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The most common form of myocarditis, endemic in both rural Central and South America, is Chagas’ disease, caused by the parasitic protozoan Trypanosoma cruzi. In North America, viral infections cause most cases of myocarditis. Enteroviruses, most importantly coxsackievirus B, are the most frequently reported cause of epidemics of viral myocarditis in children.5,11–13 However, more recent reports9,14,15 indicated that adenoviral infection is as common a cause as enteroviral infection is, if not more so. Rarely, bacteria, fungi, protozoa, parasites, and rickettsiae are causative agents. Myocarditis has also been associated with immune-mediated diseases, collagen vascular diseases, and toxins (Table 1).
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Epidemiology
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Occurrence of myocarditis can be affected by viral epidemics.7,16 An outbreak of coxsackievirus B in Europe in 1965 correlated with cardiac dysfunction in 5% of infected patients. Incidences were as high as 12% that same year in Scotland, Finland, and Austria.11 Seasonal viral distributions have been recognized for decades (influenza prevalent during winter months; poliovirus and coxsackievirus A and B typically isolated during summer and fall). Myocarditis has been a prominent finding during epidemics of influenza; thus, occurrence may be seasonal.7
Age plays a marked role in prevalence. During the neonatal period, myocarditis is usually abrupt, severe, and often fatal, with mortality as high as 75%.11,12 Infants infected with coxsackievirus B during the first year of life have a high incidence of myocarditis. Myocarditis has been linked to sudden infant death syndrome, because inflammatory infiltrates have been found on autopsies of some victims.2 Incidence increases again during late childhood and adolescence; the myocarditis usually has a delayed onset and patients recover.7
Male predominance has been noted with coxsackievirus B heart disease, particularly in adolescents and adults. In these age groups, two-thirds to three-quarters of patients with myocarditis are male.7 Male predominance has also been reported with coxsackievirus A myocarditis and poliomyelitis. Whether or not differences between the sexes occur in other viral infections is unknown.7
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Pathophysiology
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Although viral infection is the most common initiator of acute myocarditis, the subsequent autoimmune response plays a lead role in myocyte injury.7,8,11,15,17 The principal mechanism of myocardial damage is not just viral replication; it includes cell-mediated immunological reactions.
The pathophysiology of myocarditis has been studied in mice infected with a cardiotropic virus, such as coxsackievirus B. After systemic infection, the virus enters the myocyte, where it replicates in the cytoplasm of the cell. Some replicated viruses then enter the interstitium and are phagocytized by activated macrophages.3,8 Macrophage activation is due to both viral particles in the interstitium and the release of interferon 
by natural killer (NK) cells. The release of interferon is followed by release of proinflammatory cytokines (interleukins 1β and 2 and tumor necrosis factor 
). When activated by interleukin 2, NK cells eliminate virally infected myocytes and inhibit virus replication11,18,19 (Figure 2). The significance of the action of NK cells in the pathogenesis of the disease is well established; in animals depleted of NK cells before infection, a more severe myocarditis develops.8
As noted earlier, myocarditis after infection with coxsackievirus B occurs more often in men. This propensity may be related to differences between the sexes in the activation of NK cells. After infection, myocarditis that develops in female mice is less severe than that in male mice. In one study,11 after the same infection, male mice were markedly less efficient than female mice in activating NK cells. This decrease in NK-cell activation presumably results in decreased viral clearance with a resultant increase in illness severity.11 This difference in NK-cell activation may explain the male predominance for the development of clinically significant myocarditis.
Unlike NK cells, T cells may contribute to damage in both infected and noninfected myocytes.5,11,20 Activation of T cells results in accumulation of macrophages within the myocyte and production of cell-mediated cytotoxic effects.7,11 Although T cells can lyse virus-infected myocytes, the accumulation of macrophages and the concomitant cytotoxic effects create a fine balance between viral clearance and myocyte damage.8 Adding to myocyte injury, lysis by T cells is indiscriminate; it occurs in both infected and noninfected cells.7,11 The result is necrosis of healthy as well as infected myocytes. Therefore, a percentage of myocardial damage comes from "friendly fire," specifically the patient’s own immune response.
Permanent myocardial damage can be the end result of myocarditis. Such damage is thought to be due to an overaggressive immunological activation in which persistent T-cell infiltration leads to long-term tissue destruction and subsequent dilated cardiomyopathy.8,18 Infection with enteroviruses plays a major role in chronic forms of dilated cardiomyopathy.21,22
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Clinical Manifestations and Diagnosis
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Myocarditis is classified as fulminant, acute, or chronic. Fulminant myocarditis is preceded by a viral prodrome that is followed by sudden onset of severe hemodynamic compromise. Acute myocarditis has a less distinct onset and, initially, less severe compromise but is followed by a worse outcome than fulminant myocarditis. McCarthy et al23 found that adults with fulminant myocarditis had excellent long-term survival, whereas patients with acute myocarditis had progressive failure that led to death or the need for a heart transplant. Chronic myocarditis can be defined as persistent (lasting >3 months), recurrent, and latent.23
Diagnosing myocarditis in children can be challenging. Not only can children have a wide range of nonspecific signs and symptoms, but depending on cognitive development, they may not be able to communicate their symptoms. Despite a variety of invasive and noninvasive studies, myocarditis is a presumptive diagnosis based on history and clinical features.5,8
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History
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Clinical features of viral myocarditis are affected by age, sex, and the child’s baseline health status. These variables affect the balance between pathogen clearance and degree of inflammation.3,11,12 Older children may have a history of upper respiratory infection; infants may have anorexia, vomiting, and lethargy.12 Often, signs and symptoms are nonspecific or may resemble the signs and symptoms of relatively common diagnoses in children, including bronchiolitis, pneumonia, failure to thrive, and gastroenteritis.5,9
Both cases described earlier had the potentially insidious manifestations of viral myocarditis. In the first case, the signs and symptoms suggested benign gastroenteritis with slight dehydration, a situation that is not unusual in toddlers and pre-school children. K.M., who had a history of gastroenteritis, also had syncope, wheezing, and increased work of breathing. His history of asthma confounded his clinical features. Consequently, he initially received treatment for an exacerbation of asthma.
Older children may have chest pain (the sole symptom in some patients).24 Some have abdominal pain. Atypical manifestations such as syncope (K.M.), seizures, and sudden death also have been reported.2,6 A more focused cardiac examination when no signs of congestive heart failure occur may be prompted by patients’ reports of chest pain, dyspnea, exercise intolerance, or fatigue. Tachycardia of unknown origin in an otherwise healthy child may be an ominous sign. Newborns and infants, unlike older children, are more likely to have circulatory shock.12
When myocarditis is suspected, a thorough history is imperative for identifying possible causes. Parents should be asked about exposures to potential infectious agents, pharmacological agents that can cause myocardial inflammation, and toxins, including illicit drugs (eg, cocaine). Immunization status should be obtained because several infectious diseases of childhood (diphtheria, poliomyelitis) are potential causes.
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Physical Examination
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During episodes of cardiac compromise, neurohormonal responses activate the sympathetic nervous system and the renin-angiotensin-aldosterone system, resulting in improved contractility, increase in heart rate, vasoconstriction, and fluid and sodium retention. Tachycardia out of proportion for age is common in children with myocardial compromise as the heart attempts to compensate for inadequate oxygen delivery to the tissues. Vasoconstriction occurs to improve preload and maintain blood pressure. This decrease in peripheral perfusion is manifested as cool extremities, described by level of coolness (eg, cool to midcalf, cool to knee), quality of pulses, capillary refill time (compromise considered at >3 seconds with the extremity at the level of the heart), decreased urine output (<1 mL/kg per hour), and changes in mental status.25,26 Pulse quality is characterized by using the 0 to 4 pulse intensity scale (0 = no pulses detected, 4 = bounding).26 Extremities may appear mottled or pale. Despite these alterations in perfusion, it must be emphasized that vasoconstriction in children will maintain a blood pressure within a normal range for age even when tissue perfusion is inadequate. Hypotension is considered not only a late finding of cardiac failure but also an ominous one.27
Often, an S3 (ventricular gallop) occurs because of rapid filling of a non-compliant, poorly contracting left ventricle. Murmurs are less common, although a soft systolic murmur may be heard if mitral or tricuspid insufficiency is present.12 Heart sounds may be muffled if concomitant pericarditis is present.11 Rhythm irregularities may be detected, especially supraventricular tachycardia or ventricular ectopic beats as with K.M.
Tachypnea is a common sign of myocardial failure in children. Tachypnea is the result of pulmonary edema due to left ventricular failure.26 Clinical findings can include wheezing, a cough, grunting, nasal flaring, and intercostal retraction. Older children may report orthopnea or inability to catch their breath. Cyanosis is rare. Rales are typically a late sign of pulmonary congestion and may not occur at all in infants.26
Hepatomegaly, an indication of venous congestion, may or may not occur. Liver tenderness or absence of a firm edge on palpation below the right costal margin may indicate liver engorgement. Clinical findings of viral myocarditis are summarized in Table 2.
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Diagnostic Evaluation
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The diagnostic approach for a child with suspected myocarditis includes strategies to both aid in establishing the diagnosis and rule out disease processes that may mimic myocarditis (eg, a structural cardiac defect or pericardial effusion). In addition, many of these interventions provide an estimate of myocardial function and can help in establishing clinical interventions. Diagnostic findings are summarized in Table 3.
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Chest Radiography
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Evidence of cardiomegaly on a chest radiograph is an important clinical finding in myocarditis; however, the degree of heart enlargement depends on the stage of the disease. Subacute or chronic myocarditis is characterized by cardiomegaly; cardiomegaly may or may not occur in children with fulminant myocarditis.12 In fact, the possibility of myocarditis is often not considered until late, when cardiomegaly is evident on chest radiographs.5 Myocarditis should not be ruled out in infants or children with marked cardiovascular compromise or collapse of unknown cause who do not have evidence of heart enlargement on radiographs.
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Electrocardiography
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Although not diagnostic, findings on an electrocardiogram are rarely normal in patients with myocarditis.5,12 Some children have such mild illness that a conduction disturbance on an electrocardiogram is the only abnormal finding.11 Sinus tachycardia is a common finding with myocarditis.12 Low-voltage QRS complexes, ST-T wave abnormalities, or prolonged QT interval may be apparent.5,11,12 Left ventricular hypertrophy with repolarization changes (strain) is typical. Complete atrioventricular block has also been described.9,11 Occasionally, evidence of myocardial infarction is seen.12
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Echocardiography
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Findings on echocardiograms are rarely normal in patients with myocarditis. As with K.M., impaired left ventricular function with dilatation of 1 or more chambers is typical. K.M.’s echocardiogram showed poor left ventricular systolic function, with dilatation and slightly diminished right ventricular function. In the absence of any structural abnormalities, these findings help establish the diagnosis.11,12 Generally, right ventricular function is less compromised than is left ventricular function; atrioventricular valve regurgitation may occur. Occasionally, left ventricular thrombi are found.12
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Laboratory Studies
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Historically, despite its limited sensitivity and specificity and its inherent risks, endomyocardial biopsy has been the reference standard for diagnosing viral myocarditis.2,15,20 Nevertheless, for several reasons, endomyocardial biopsy is used less often in children than in adults.9 First, biopsy can be associated with significant sampling error.24,28 Several tissue specimens (5 or more) are needed because of the focal nature of the disease; many clinicians think that biopsy leads to underestimation of the presence of the disease.24,28 Second, borderline myocarditis can result in little to no evidence of myocyte destruction.1 Third, expert interpretation can vary, including variance with other markers of viral infection.2,8,24,28 Because of the possibility of false-negative results, lack of an endomyocardial biopsy positive for myocarditis does not rule out this disease.
For K.M., findings on endomyocardial biopsy on hospital day 8 confirmed the diagnosis. Tissue specimens from the right ventricle had intact myocytes with small foci of lymphocytic infiltrates and extensive areas of myocyte destruction with organizing fibrosis and infiltrates of inflammatory cells most consistent with myocarditis.
Recently, use of less invasive means of diagnosing myocarditis in children has been emphasized.2 Use of polymerase chain reaction (PCR) and in situ hybridization has increased the sensitivity for diagnosing viral myocarditis.3,5,13,19,29 Tracheal aspirates for PCR analysis in intubated children are useful for detecting viral genomes in children with or without myocarditis. Akhtar et al30 reported that PCR of tracheal aspirates had a sensitivity of 100% for predicting the results of PCR of endomyocardial biopsy specimens, albeit for a small (n = 10) sample size. Although a tracheal aspirate positive for virus is not diagnostic for myocarditis itself, PCR of tracheal aspirates may provide a safer means of identifying a viral cause for illness in children with cardiac decompensation of unknown origin.30
Serological studies may reveal an elevation in myocardial enzyme levels (creatine kinase, normal value 25–190 IU/L [to convert to microkatals, multiply by 0.0167]; MB isoenzyme of creatine kinase, normal value <12% of creatine kinase).12 In children, the level of cardiac troponin T is a more sensitive indicator of myocardial damage than are myocardial enzyme levels.5,12,26 In healthy children, cardiac troponin levels are typically less than the detection level (<0.02 ng/mL). Lauer et al31 reported that 35% of patients with suspected myocarditis also had elevated levels of cardiac troponin; among those, 98% had viral myocarditis confirmed histologically.
Other nonspecific laboratory studies may aid in the diagnosis of viral myocarditis. Elevations in sedimentation rate (>20 mm/h) and level of C-reactive protein (>0.05 mg/dL; to convert to nanomoles per liter, multiply by 9.524) may occur. A normal sedimentation rate, however, does not rule out myocarditis. Viral studies may reveal enteroviral or adenoviral antibodies, Esptein-Barr virus, cytomegalovirus, or a 4-fold increase in the level of immunoglobulin G but do not definitively establish causation.3,5,20 Levels of immunoglobulin G antibodies to Epstein-Barr virus nuclear antigen were elevated in K.M. PCR may also be used to detect viral genomes.
Elevation in white blood cell count with predominance of lymphocytes may suggest viral causes of myocarditis. Cultures of blood, stool, cerebrospinal fluid, or nasopharyngeal secretions are less specific than cultures of tracheal aspirates; Martin et al13 found that cultures showed growth in only 27% of children with viral myocarditis.
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Critical Care Management
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Care of children with clinical features consistent with myocarditis depends on the severity of myocardial dysfunction. Management is designed around supportive measures rather than being aimed at a causative agent. Maintenance of cardiac output with aggressive support of cardiac function is essential. Such support includes initiation and monitoring of inotropic therapy, afterload reduction, arrhythmia management, and adequate tissue oxygenation. Respiratory support may require intubation and mechanical ventilation. Fluid management may include both administration of fluid boluses and diuretic therapy. Monitoring of and interventions to prevent complications should be ongoing.
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Inotropic Support
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When cardiac output is inadequate, a rapid acting inotropic agent is administered.11,12,26 Inotropic agents are administered cautiously because the myocardium is irritable and use of inotropic agents can instigate and/or worsen arrhythmias. One inotropic agent or a combination of such agents, including dopamine, dobutamine, and milrinone, can be administered (Table 4).
Dobutamine is often used when the primary cause of inadequate tissue perfusion is cardiac in origin. Dobutamine improves contractility and decreases systemic vascular resistance, providing afterload reduction in addition to improving cardiac output. A mild increase in heart rate can occur, although significant tachycardia is unusual. Although dobutamine increases myocardial oxygen demand in adults with congestive heart failure, in children with patent coronary arteries, coronary blood flow and oxygen supply to the heart actually increase.29
Dopamine has both inotropic and vasopressor properties and is useful in patients who are in shock with cardiac dysfunction and associated mild to moderate hypotension. Dopamine is not routinely used to tidal volume (pressure ventilation), a decrease in oxygen saturation, and asymmetric chest rise. If the tube migrates into the right main bronchus, the child should immediately be placed back in the previous position and reassessed. Breath sounds should be assessed after any change in body position.
Neck extension increases airway length, potentially causing unintentional extubation because the uncuffed tube can easily pass upward through the vocal cords. Immediate respiratory distress, decrease in oxygen saturation, marked decrease in or undetectable end-tidal carbon dioxide levels, grunting, or vocalization can indicate possible inadvertent extubation. If dislodgement of the endotracheal tube into the esophagus is suspected, the tube should be removed and bag-valve-mask ventilation performed until reintubation or effective spontaneous breathing occurs.
Although a common practice in intensive care units, endotracheal suctioning should not be performed routinely.44 Suctioning can be associated with complications, including hypoxemia, bradycardia, atelectasis, and dysrhythmias. Suctioning should be done on an as-needed basis rather than routinely. Indications for suctioning include increase in airway pressure, decrease in tidal volume, decrease in oxygen saturation, visualization of secretions in the tube, development of rhonchi, and coughing. Hyperoxygenation may or may not be required before suctioning, depending on the child’s arterial oxygenation and tolerance to the procedure. The catheter should not be deeper than the end of the endotracheal tube. Catheters inserted to the point of resistance (carina) cause tissue inflammation and damage.45 Instillation of normal saline for lavage should be avoided because that practice is not supported by research and may actually be harmful.44,45
Routine bedside nursing interventions such as dressing changes, bathing, weighing, and repositioning all significantly increase tissue oxygen consumption. Delay in carrying out these procedures may be necessary. Conversely, some or all of these activities may be clustered if tolerated in order to allow longer periods of rest.
Fever increases oxygen consumption 10% for each 1°C elevation in body temperature. Although not all fever is "bad," treatment of fever is recommended in children with cardiopulmonary disease. Attempts should be made to maintain normothermia.26 Unless contraindicated, antipyretics (acetaminophen, ibuprofen) should be administered. Fever reduction can also be attempted with external cooling, usually by sponging with tepid water.
Pain and anxiety significantly increase oxygen demand and consumption and cause considerable distress for children in the PICU. Assessment and management of pain and anxiety should be ongoing.
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Arrhythmias
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Heart rate and rhythm require monitoring. Arrhythmias are a significant life-threatening complication of myocarditis.24 Development of bradycardia or tachyarrhythmias is unlikely to be tolerated and requires immediate recognition and treatment.
Infants and small children depend on heart rate for adequate cardiac output because stroke volume is relatively fixed; in young children, bradycardia can rapidly diminish cardiac output. Because chronotropic drugs can induce ventricular tachycardia in patients with viral myocarditis, cardiac pacing is the preferred treatment for life-threatening bradyarrhythmias, including atrioventricular block.25
Transcutaneous or transthoracic pacing is a noninvasive procedure that can be done rapidly. Two electrodes are placed on the patient with the anterior electrode in the V2 to V5 position and the posterior electrode under the scapula to the left of the spine. Electrode adherence should be checked frequently, especially if the child is diaphoretic. If needed for prolonged periods, electrodes should be changed a minimum of every 24 hours to maintain effectiveness of the contact gel.
For ongoing bradyarrhythmias, invasive pacing should be considered. Transvenous leads are placed percutaneously via a large vessel into the right atrium or ventricle. Leads are stiff; nurses must be alert for indications of ventricular perforation, including cardiac tamponade. An extra battery should be kept at the bedside of any patient who is pacemaker dependent. Hospital policy should be followed when caring for the insertion site and catheter.
| Sidebar As a general rule, for children more than 1 year old, estimated systolic blood pressure norms can be calculated as follows:
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Conversely, an excessively rapid heart rate will decrease ventricular filling time, resulting in inadequate preload and subsequent cardiac output. Tachycardias also result in inadequate coronary artery filling time. Coronary arteries fill and perfuse the myocardium during diastole; the faster the heart rate, the shorter is diastole, leading to a decrease in myocardial oxygen supply during a time of increasing consumption.
Differentiation between sinus tachycardia and supraventricular tachycardia is critical. Typically, sinus tachycardia is heart rate greater than 140/min in children, greater than 160/min in infants, and varies from beat to beat. Heart rate generally remains less than 200/min. Sinus tachycardia can be the result of a variety of factors, including fear, anxiety, fever, pain, intravascular dehydration, and marked vasodilatation. Sinus tachycardia will resolve, or partially resolve, with resolution of the inciting factor.
Supraventricular tachycardia is an extremely rapid heart rate (200–280/min); is unresponsive to resolution of fever, pain, hypovolemia, and so on; and has no beat-to-beat variability. Rates of sinus tachycardia and supraventricular tachycardia can overlap, making determination of the type of tachycardia difficult. A 12-lead electrocardiogram may be necessary to differentiate between the two. Once supraventricular tachycardia has been established, rapid treatment with adenosine in the patients with stable hemodynamic status or cardioversion in patients with unstable hemodynamic status is performed. A defibrillator should remain near any child who has myocarditis or recurring supraventricular tachycardia.
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Hemodynamic Monitoring
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Case 1
Case 2
