Sie sind auf Seite 1von 24

PediatricCare

Viral
Myocarditis Although myocarditis severe enough
to be recognized is rare, it is the
or diarrhea. One day before the visit
to the emergency department, he
most common cause of heart failure had been vomiting and had been
in Children in otherwise healthy children.4 In unable to tolerate anything by mouth.
both children and adults, most cases On arrival in the emergency
Tammy L. Uhl, RN, MSN, are subclinical; thus, the true inci- department, A.J. appeared ill but
CCRN, CCNS dence of myocarditis in children is was alert and in no marked distress.
unknown.2,5-7 Unfortunately, the clini- Vital signs were heart rate, 162/min;
cal features of myocarditis can vary respirations, 26/min; and oxygen
widely, and often no cardiac signs saturation, determined by pulse
or symptoms occur, complicating oximetry, 99% on room air. No
recognition. For children in whom murmur or gallop was noted; capil-
the diagnosis is suspected or cardio- lary refill was brisk with 2+ periph-
vascular compromise is severe enough eral pulses and warm extremities.
This article has been designated for CE credit. to require admission to the pedi- Breath sounds were clear bilater-
A closed-book, multiple-choice examination
follows this article, which tests your knowledge atric intensive care unit (PICU), crit- ally. He appeared mildly dehy-
of the following objectives: ical care nurses are an essential drated with tachycardia, mildly
1. Identify which population is at most risk of component in determining manage- sunken eyes, and tacky mucous
death as the result of myocarditis
2. Identify the mechanism that results in
ment, care, and outcomes. In this membranes.
morbidity and mortality in children with article, I describe the etiology of viral Routine blood tests were done.
myocarditis
3. Discuss the signs and symptoms of
myocarditis in children, potential Electrolyte levels were normal
myocarditits in children insidious clinical features, patho- except for a carbon dioxide level of
4. Describe the treatment of patients with physiology of the disease, and critical 18 mEq/L, an anion gap of 23 mEq/L,
myocarditis
care management. and a serum urea nitrogen level of
21 mg/dL (to convert to millimoles
Case 1 per liter, multiply by 0.357), consis-

M yocarditis is defined as
inflammation of the myocardium
followed by necrosis and/or degen-
A.J., a previously healthy 3-year-
old boy, was brought to the emer-
gency department because his body
temperature was 40.5ºC. During the
previous week, he had had some
tent 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
eration of myocytes.1-3 The inflam- nasal discharge and a mild, nonpro- count of 321000/μL. A differential
mation can be diffuse or focal and is ductive cough. He had no history of count was not completed.
usually due to an infection. increased work of breathing, rashes, Approximately 15 minutes after
his initial examination, A.J. received
two 20 mL/kg intravenous boluses
Author of normal saline and was given some-
Tammy L. Uhl is a pediatric critical care clinical nurse specialist at Brenner Children’s thing to eat, which he tolerated well.
Hospital, Wake Forest University Baptist Medical Center, Winston-Salem, North
Carolina. Because his parents were comfort-
Corresponding author: Tammy L. Uhl, RN, MSN, CCRN, CCNS, Brenner Children’s Hospital, Wake Forest University able with observing the child at
Baptist Medical Center, Medical Center Blvd, Winston-Salem, NC 27157 (e-mail: tuhl@wfubmc.edu). home and expressed full under-
To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. standing of the signs of dehydration,
Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org.
A.J. was readied for discharge.

42 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 http://ccn.aacnjournals.org

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019


While the discharge papers were ograph and continuing respiratory Incidence and Prevalence
being completed, A.J. suddenly deterioration, he was intubated and Myocarditis appears to be more
became unresponsive and apneic. mechanical ventilation was started. common in children than in adults.8
Bag-valve-mask ventilation was begun, Within minutes of intubation, clini- Its true incidence, however, is
and subsequently he was pulseless. cally significant unifocal premature unknown; it is thought that subclini-
Cardiopulmonary resuscitation was ventricular contractions and hypoten- cal cases (“silent” myocarditis) occur
initiated. After a prolonged attempt sion (50-60/20-30 mm Hg) devel- much more often than do severe
at resuscitation, he was pronounced oped. He was given a lidocaine bolus, cases. Many cases are unrecognized
dead. Postmortem examination and continuous infusions of both because of the wide range of signs and
revealed myocarditis of probable lidocaine and epinephrine were symptoms and, in some patients, the
viral origin. started. Laboratory studies revealed complete lack of clinical findings.8,9 In
a white blood cell count of 7300/μL, a postmortem study of children who
Case 2 a hemoglobin level of 11.1 g/dL, a died without a history suggestive of
K.M., a 5-year-old boy with a platelet count of 103000/μL, and myocarditis, researchers found evi-
history of asthma, was brought to unremarkable electrolyte levels. An dence of active or healed myocarditis
the emergency department because echocardiogram showed markedly in 17 of 138 cases (12.3%).8,10 Of the 17
he had fainted. After the syncopal decreased left ventricular function cases, 15 occurred in children who
episode, he had shortness of breath with an ejection fraction of 10% to died suddenly. In postmortem studies
and tachypnea. Approximately 4 days 14% and diminished right ventricu- in adults, myocardial inflammation
before this visit to the emergency lar function. Neither structural occurred in 1% to 9%.8
department, he had had gastroen- abnormalities nor pericardial effu-
teritis with vomiting and diarrhea sion was seen. A 12-lead electrocar- Etiology
that resolved. Findings on a physical diogram showed a normal sinus The most common form of
examination were unremarkable rhythm with frequent premature myocarditis, endemic in both rural
except for bilateral wheezing and ventricular contractions and non- Central and South America, is Cha-
increased work of breathing. He was specific T-wave abnormalities (Fig- gas’ disease, caused by the parasitic
given several albuterol nebulizers for ure 1). The diagnosis was acute protozoan Trypanosoma cruzi. In
a suspected exacerbation of asthma. myocarditis with severe cardiomy- North America, viral infections cause
A chest radiograph revealed bilateral opathy. Because of the continued most cases of myocarditis. Entero-
infiltrates thought to be consistent deterioration in K.M.’s condition, viruses, most importantly coxsack-
with Mycoplasma pneumonia. He was inability to oxygenate, and worsen- ievirus B, are the most frequently
given azithromycin and was trans- ing cardiac function, extracorporeal reported cause of epidemics of viral
ferred to a tertiary care center for membrane oxygenation (ECMO) myocarditis in children.5,11-13 How-
closer observation. was started. ever, more recent reports9,14,15 indi-
On arrival in the PICU, his respi- ECMO was discontinued on cated that adenoviral infection is as
ratory status continued to deteriorate. hospital day 13. K.M. made steady common a cause as enteroviral
He was markedly tachypneic. Oxygen improvement, although he continued infection is, if not more so. Rarely,
saturations were 86% to 91% on a to require vasoactive support and bacteria, fungi, protozoa, parasites,
100% nonrebreather mask. Continu- mechanical ventilation for another and rickettsiae are causative agents.
ous albuterol was begun, but his 6 days. He was extubated on hospital Myocarditis has also been associated
pulmonary status did not change. day 19. At that time, his ejection with immune-mediated diseases,
Auscultation revealed diminished fraction was approximately 35%. He collagen vascular diseases, and tox-
breath sounds at the bases bilaterally, was subsequently transferred to the ins (Table 1).
no wheezing, and no murmur but a pediatric rehabilitation unit, from
gallop. A repeat chest radiograph which he eventually was discharged Epidemiology
revealed pulmonary edema and to home; the diagnosis was severe Occurrence of myocarditis can
cardiomegaly. After the repeat radi- dilated cardiomyopathy. be affected by viral epidemics.7,16 An

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 43


Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019
PediatricCare

aVR V1 V4

aVL V2 V5

aVF V3 V6

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.

outbreak of coxsackievirus B in drome, because inflammatory infil- autoimmune response plays a lead
Europe in 1965 correlated with car- trates have been found on autopsies role in myocyte injury.7,8,11,15,17 The
diac dysfunction in 5% of infected of some victims.2 Incidence increases principal mechanism of myocardial
patients. Incidences were as high as again during late childhood and damage is not just viral replication;
12% that same year in Scotland, Fin- adolescence; the myocarditis usually it includes cell-mediated immuno-
land, and Austria.11 Seasonal viral has a delayed onset and patients logical reactions.
distributions have been recognized recover.7 The pathophysiology of
for decades (influenza prevalent Male predominance has been myocarditis has been studied in
during winter months; poliovirus noted with coxsackievirus B heart mice infected with a cardiotropic
and coxsackievirus A and B typically disease, particularly in adolescents virus, such as coxsackievirus B.
isolated during summer and fall). and adults. In these age groups, two- After systemic infection, the virus
Myocarditis has been a prominent thirds to three-quarters of patients enters the myocyte, where it repli-
finding during epidemics of influenza; with myocarditis are male.7 Male cates in the cytoplasm of the cell.
thus, occurrence may be seasonal.7 predominance has also been reported Some replicated viruses then enter
Age plays a marked role in preva- with coxsackievirus A myocarditis the interstitium and are phagocy-
lence. During the neonatal period, and poliomyelitis. Whether or not tized by activated macrophages.3,8
myocarditis is usually abrupt, severe, differences between the sexes occur Macrophage activation is due to
and often fatal, with mortality as in other viral infections is unknown.7 both viral particles in the intersti-
high as 75%.11,12 Infants infected with tium and the release of interferon γ
coxsackievirus B during the first Pathophysiology by natural killer (NK) cells. The
year of life have a high incidence of Although viral infection is the release of interferon γ is followed by
myocarditis. Myocarditis has been most common initiator of acute release of proinflammatory cytokines
linked to sudden infant death syn- myocarditis, the subsequent (interleukins 1β and 2 and tumor

44 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 http://ccn.aacnjournals.org

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019


infected myocytes, the accumula-
Table 1 Causes of myocarditis
tion of macrophages and the con-
Viruses Immune-mediated diseases Drugs
comitant cytotoxic effects create a
Coxsackievirus A Rheumatoid arthritis Sulfonamides fine balance between viral clearance
Coxsackievirus B Rheumatic fever Cyclophosphamide and myocyte damage.8 Adding to
Echovirus Ulcerative colitis Acetazolamide myocyte injury, lysis by T cells is
Adenovirus Systemic ulcerative colitis Amphotericin B indiscriminate; it occurs in both
Rubella virus Indomethacin infected and noninfected cells.7,11
Toxins The result is necrosis of healthy as
Measles virus Tetracycline
Ethanol well as infected myocytes. There-
Varicella virus Phenytoin
Heavy metals: iron, copper, lead fore, a percentage of myocardial
Poliovirus Penicillin
Mumps virus
Arsenic damage comes from “friendly fire,”
Bee and wasp stings Fungi and yeast specifically the patient’s own
Herpesvirus
Carbon monoxide Aspergillus immune response.
Epstein-Barr virus
Scorpion bites Candida Permanent myocardial damage
Cytomegalovirus
Spider bites can be the end result of myocardi-
Arbovirus
Snake bites
Protozoa tis. Such damage is thought to be
Influenza virus
Trypanosoma cruzi due to an overaggressive immuno-
Human immunodeficiency logical activation in which persistent
Physical conditions or agents Toxoplasma gondii
virus
Hyperpyrexia T-cell infiltration leads to long-term
Parasites tissue destruction and subsequent
Bacteria Electric shock
Meningococci Radiation
Ascaris dilated cardiomyopathy.8,18 Infection
Schistosoma with enteroviruses plays a major
Borrelia burgdorferi
(Lyme disease) Trichinella spiralis role in chronic forms of dilated
Salmonellae cardiomyopathy.21,22
Mycobacteria
Streptococci
Clinical Manifestations and
Diagnosis
Myocarditis is classified as ful-
necrosis factor α). When activated infection, male mice were markedly minant, acute, or chronic. Fulmi-
by interleukin 2, NK cells eliminate less efficient than female mice in nant myocarditis is preceded by a
virally infected myocytes and inhibit activating NK cells. This decrease in viral prodrome that is followed by
virus replication11,18,19 (Figure 2). The NK-cell activation presumably results sudden onset of severe hemody-
significance of the action of NK cells in decreased viral clearance with a namic compromise. Acute myocardi-
in the pathogenesis of the disease is resultant increase in illness severity.11 tis has a less distinct onset and,
well established; in animals depleted This difference in NK-cell activation initially, less severe compromise
of NK cells before infection, a more may explain the male predominance but is followed by a worse outcome
severe myocarditis develops.8 for the development of clinically sig- than fulminant myocarditis.
As noted earlier, myocarditis nificant myocarditis. McCarthy et al23 found that adults
after infection with coxsackievirus B Unlike NK cells, T cells may with fulminant myocarditis had
occurs more often in men. This contribute to damage in both infected excellent long-term survival, whereas
propensity may be related to differ- and noninfected myocytes.5,11,20 patients with acute myocarditis had
ences between the sexes in the acti- Activation of T cells results in accu- progressive failure that led to death
vation of NK cells. After infection, mulation of macrophages within or the need for a heart transplant.
myocarditis that develops in female the myocyte and production of cell- Chronic myocarditis can be defined
mice is less severe than that in male mediated cytotoxic effects.7,11 as persistent (lasting >3 months),
mice. In one study,11 after the same Although T cells can lyse virus- recurrent, and latent.23

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 45


Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019
PediatricCare

Prodromal viral illness

Viral invasion of myocyte Release of interferon by natural killer cells

Viral replication, release


into interstitium
Activation of macrophages

Myocyte death
Viral phagocytosis Release of interleukins 1β and 2, tumor necrosis factor

Activation of natural killer cells


Activation of T cells

Elimination of infected
myocytes
Lysis of infected Lysis of noninfected
myocytes myocytes
Inhibition of viral replication

Myocardial inflammation and/or damage

Full recovery

Death Survival Recovery with residual


myocardial dysfunction

Recovery with marked


dilated cardiomyopathy
Figure 2 Pathophysiology of myocarditis.

Diagnosing myocarditis in chil- may have anorexia, vomiting, and received treatment for an exacerba-
dren can be challenging. Not only lethargy.12 Often, signs and symp- tion of asthma.
can children have a wide range of toms are nonspecific or may resem- Older children may have chest
nonspecific signs and symptoms, ble the signs and symptoms of pain (the sole symptom in some
but depending on cognitive devel- relatively common diagnoses in patients).24 Some have abdominal
opment, they may not be able to children, including bronchiolitis, pain. Atypical manifestations such
communicate their symptoms. pneumonia, failure to thrive, and as syncope (K.M.), seizures, and
Despite a variety of invasive and gastroenteritis.5,9 sudden death also have been
noninvasive studies, myocarditis is a Both cases described earlier had reported.2,6 A more focused cardiac
presumptive diagnosis based on his- the potentially insidious manifesta- examination when no signs of con-
tory and clinical features.5,8 tions of viral myocarditis. In the first gestive heart failure occur may be
case, the signs and symptoms sug- prompted by patients’ reports of
History gested benign gastroenteritis with chest pain, dyspnea, exercise intol-
Clinical features of viral slight dehydration, a situation that erance, or fatigue. Tachycardia of
myocarditis are affected by age, sex, is not unusual in toddlers and pre- unknown origin in an otherwise
and the child’s baseline health sta- school children. K.M., who had a healthy child may be an ominous
tus. These variables affect the bal- history of gastroenteritis, also had sign. Newborns and infants, unlike
ance between pathogen clearance syncope, wheezing, and increased older children, are more likely to
and degree of inflammation.3,11,12 work of breathing. His history of have circulatory shock.12
Older children may have a history asthma confounded his clinical When myocarditis is suspected,
of upper respiratory infection; infants features. Consequently, he initially a thorough history is imperative for

46 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 http://ccn.aacnjournals.org

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019


identifying possible causes. Parents inadequate. Table 2 Myocarditis in children: clinical findings
should be asked about exposures to Hypotension is
Subjective Chest pain
potential infectious agents, phar- considered not
Abdominal pain
macological agents that can cause only a late find-
Dyspnea/orthopnea
myocardial inflammation, and tox- ing of cardiac
ins, including illicit drugs (eg, failure but also Exercise intolerance

cocaine). Immunization status an ominous Fatigue


should be obtained because several one.27 Objective Tachycardia
infectious diseases of childhood Often, an S3 Tachypnea
(diphtheria, poliomyelitis) are (ventricular Wheezing, cough, increased work of breathing
potential causes. gallop) occurs Alteration in peripheral perfusion
because of rapid Prolonged capillary refill
Physical Examination filling of a non- Decrease in pulse quality
During episodes of cardiac com- compliant, Extremity coolness
promise, neurohormonal responses poorly contract- Paleness, mottling
activate the sympathetic nervous ing left ventricle.
Decreased urine output
system and the renin-angiotensin- Murmurs are
Murmura
aldosterone system, resulting in less common,
Gallop
improved contractility, increase in although a soft
Rhythm irregularities
heart rate, vasoconstriction, and systolic murmur
fluid and sodium retention. Tachy- may be heard if Ventricular ectopy

cardia out of proportion for age is mitral or tricus- Atrioventricular block


common in children with myocar- pid insufficiency Sinus tachycardia or supraventricular tachycardia
12 a
dial compromise as the heart attempts is present. Hepatomegaly
to compensate for inadequate oxy- Heart sounds Rales b

gen delivery to the tissues. Vasocon- may be muffled Hypotensionb


striction occurs to improve preload if concomitant a May or may not be present.
and maintain blood pressure. This pericarditis is b Late finding.

11
decrease in peripheral perfusion is present.
manifested as cool extremities, Rhythm irregularities may be occur. Liver tenderness or absence
described by level of coolness (eg, detected, especially supraventricular of a firm edge on palpation below
cool to midcalf, cool to knee), qual- tachycardia or ventricular ectopic the right costal margin may indicate
ity of pulses, capillary refill time beats as with K.M. liver engorgement. Clinical findings
(compromise considered at >3 sec- Tachypnea is a common sign of of viral myocarditis are summarized
onds with the extremity at the level myocardial failure in children. in Table 2.
of the heart), decreased urine output Tachypnea is the result of pulmonary
(<1 mL/kg per hour), and changes edema due to left ventricular Diagnostic Evaluation
in mental status.25,26 Pulse quality is 26
failure. Clinical findings can include The diagnostic approach for a
characterized by using the 0 to 4 pulse wheezing, a cough, grunting, nasal child with suspected myocarditis
intensity scale (0 = no pulses detected, flaring, and intercostal retraction. includes strategies to both aid in
4 = bounding).26 Extremities may Older children may report orthop- establishing the diagnosis and rule
appear mottled or pale. Despite these nea or inability to catch their breath. out disease processes that may
alterations in perfusion, it must be Cyanosis is rare. Rales are typically a mimic myocarditis (eg, a structural
emphasized that vasoconstriction late sign of pulmonary congestion cardiac defect or pericardial effu-
in children will maintain a blood and may not occur at all in infants. 26
sion). In addition, many of these
pressure within a normal range for Hepatomegaly, an indication of interventions provide an estimate
age even when tissue perfusion is venous congestion, may or may not of myocardial function and can

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 47


Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019
PediatricCare

help in establishing clinical interven- left ventricular Table 3 Myocarditis in children: diagnostic findings
tions. Diagnostic findings are sum- function with
marized in Table 3. dilatation of 1 or Assessment Finding
more chambers is Chest radiography Cardiomegalya
Chest Radiography typical. K.M.’s Electrocardiography Tachycardia: sinus or supraventricular
Evidence of cardiomegaly on a echocardiogram Atrioventricular blocka
chest radiograph is an important clin- showed poor left Low-voltage QRS complexes
ical finding in myocarditis; however, ventricular sys-
ST-T wave abnormalities
the degree of heart enlargement tolic function, (elevation or depression)
depends on the stage of the disease. with dilatation Prolonged QT interval
Subacute or chronic myocarditis is and slightly Ventricular ectopy
characterized by cardiomegaly; car- diminished right Echocardiography Impaired ventricular function (left > right)
diomegaly may or may not occur in ventricular func- Ventricular dilatation
children with fulminant myocarditis.12 tion. In the
Atrioventricular valve regurgitationa
In fact, the possibility of myocarditis absence of any
Left ventricular thrombia
is often not considered until late, structural abnor-
Laboratory studies
when cardiomegaly is evident on malities, these
Serological tests Increased levels of creatine kinase and
chest radiographs.5 Myocarditis findings help its MB isoenzyme
should not be ruled out in infants or establish the diag-
Increased level of cardiac troponin C
children with marked cardiovascular nosis.11,12 Gener-
Elevated sedimentation ratea
compromise or collapse of unknown ally, right
Increased level of C reactive proteina
cause who do not have evidence of ventricular func-
Increased level of white blood cells,
heart enlargement on radiographs. tion is less com- with lymphocytes predominating
promised than is
Viral titersa
Electrocardiography left ventricular
Increased level of immunoglobulin Ga
Although not diagnostic, findings function; atri-
Cultures: blood, Presence of virusa
on an electrocardiogram are rarely oventricular valve stool, cerebro-
normal in patients with myocardi- regurgitation may spinal fluid,
tis.5,12 Some children have such mild occur. Occasion- nasopharyngeal
secretions
illness that a conduction distur- ally, left ventricu-
Myocardial biopsy Myocyte destruction, fibrosis, inflammatory
bance on an electrocardiogram is lar thrombi are cells, lymphocytic infiltrates
the only abnormal finding.11 Sinus found.12 a May or may not be present.
tachycardia is a common finding
with myocarditis.12 Low-voltage Laboratory
QRS complexes, ST-T wave abnor- Studies focal nature of the disease; many cli-
malities, or prolonged QT interval Historically, despite its limited nicians think that biopsy leads to
may be apparent.5,11,12 Left ventricu- sensitivity and specificity and its underestimation of the presence of
lar hypertrophy with repolarization inherent risks, endomyocardial the disease.24,28 Second, borderline
changes (strain) is typical. Complete biopsy has been the reference stan- myocarditis can result in little to no
atrioventricular block has also been dard for diagnosing viral myocardi- evidence of myocyte destruction.1
described.9,11 Occasionally, evidence tis.2,15,20 Nevertheless, for several Third, expert interpretation can vary,
of myocardial infarction is seen.12 reasons, endomyocardial biopsy is including variance with other mark-
used less often in children than in ers of viral infection.2,8,24,28 Because of
Echocardiography adults.9 First, biopsy can be associ- the possibility of false-negative
Findings on echocardiograms ated with significant sampling results, lack of an endomyocardial
are rarely normal in patients with error.24,28 Several tissue specimens (5 biopsy positive for myocarditis does
myocarditis. As with K.M., impaired or more) are needed because of the not rule out this disease.

48 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 http://ccn.aacnjournals.org

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019


For K.M., findings on endomy- Lauer et al31 reported that 35% of afterload reduction, arrhythmia
ocardial biopsy on hospital day 8 patients with suspected myocarditis management, and adequate tissue
confirmed the diagnosis. Tissue also had elevated levels of cardiac tro- oxygenation. Respiratory support
specimens from the right ventricle ponin; among those, 98% had viral may require intubation and
had intact myocytes with small foci myocarditis confirmed histologically. mechanical ventilation. Fluid man-
of lymphocytic infiltrates and exten- Other nonspecific laboratory agement may include both admin-
sive areas of myocyte destruction studies may aid in the diagnosis of istration of fluid boluses and
with organizing fibrosis and infil- viral myocarditis. Elevations in sedi- diuretic therapy. Monitoring of
trates of inflammatory cells most mentation rate (>20 mm/h) and level and interventions to prevent com-
consistent with myocarditis. of C-reactive protein (>0.05 mg/dL; plications should be ongoing.
Recently, use of less invasive to convert to nanomoles per liter,
means of diagnosing myocarditis multiply by 9.524) may occur. A Inotropic Support
in children has been emphasized.2 normal sedimentation rate, however, When cardiac output is inade-
Use of polymerase chain reaction does not rule out myocarditis. Viral quate, a rapid acting inotropic
(PCR) and in situ hybridization has studies may reveal enteroviral or agent is administered.11,12,26
increased the sensitivity for diagnos- adenoviral antibodies, Esptein-Barr Inotropic agents are administered
ing viral myocarditis.3,5,13,19,29 Tracheal virus, cytomegalovirus, or a 4-fold cautiously because the myocardium
aspirates for PCR analysis in intu- increase in the level of immuno- is irritable and use of inotropic
bated children are useful for detect- globulin G but do not definitively agents can instigate and/or worsen
ing viral genomes in children with establish causation.3,5,20 Levels of arrhythmias. One inotropic agent
or without myocarditis. Akhtar et immunoglobulin G antibodies to or a combination of such agents,
al30 reported that PCR of tracheal Epstein-Barr virus nuclear antigen including dopamine, dobutamine,
aspirates had a sensitivity of 100% were elevated in K.M. PCR may also and milrinone, can be administered
for predicting the results of PCR of be used to detect viral genomes. (Table 4).
endomyocardial biopsy specimens, Elevation in white blood cell Dobutamine is often used when
albeit for a small (n = 10) sample count with predominance of lym- the primary cause of inadequate
size. Although a tracheal aspirate phocytes may suggest viral causes tissue perfusion is cardiac in origin.
positive for virus is not diagnostic of myocarditis. Cultures of blood, Dobutamine improves contractility
for myocarditis itself, PCR of tracheal stool, cerebrospinal fluid, or and decreases systemic vascular
aspirates may provide a safer means nasopharyngeal secretions are less resistance, providing afterload
of identifying a viral cause for illness specific than cultures of tracheal reduction in addition to improving
in children with cardiac decompen- aspirates; Martin et al13 found that cardiac output. A mild increase in
sation of unknown origin.30 cultures showed growth in only 27% heart rate can occur, although sig-
Serological studies may reveal of children with viral myocarditis. nificant tachycardia is unusual.
an elevation in myocardial enzyme Although dobutamine increases
levels (creatine kinase, normal Critical Care Management myocardial oxygen demand in adults
value 25-190 IU/L [to convert to Care of children with clinical with congestive heart failure, in
microkatals, multiply by 0.0167]; features consistent with myocarditis children with patent coronary
MB isoenzyme of creatine kinase, depends on the severity of myocar- arteries, coronary blood flow and
normal value <12% of creatine dial dysfunction. Management is oxygen supply to the heart actually
kinase).12 In children, the level of designed around supportive meas- increase.29
cardiac troponin T is a more sensi- ures rather than being aimed at a Dopamine has both inotropic
tive indicator of myocardial damage causative agent. Maintenance of car- and vasopressor properties and is
than are myocardial enzyme lev- diac output with aggressive support useful in patients who are in shock
els.5,12,26 In healthy children, cardiac of cardiac function is essential. Such with cardiac dysfunction and asso-
troponin levels are typically less than support includes initiation and ciated mild to moderate hypotension.
the detection level (<0.02 ng/mL). monitoring of inotropic therapy, Dopamine is not routinely used to

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 49


Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019
PediatricCare

Table 4 Continuous infusion inotropic support

Drug Classification Dose, µg/kg per minute Actiona Adverse effects


Dopamine Sympathomimetic 0.5-2 Dopaminergic: Tachyarrhythmias
renal vasodilatation
Promotion of sodium Reduced renal blood flow
excretion at >5 µg/kg per minute

5-10 ß1-adrenergic effects Increased myocardial oxygen


demand
10-15 Mixed α1-, ß1-adrenergic effects
>20 Predominantly α1-adrenergic Ectopy
effects
Dobutamine Sympathomimetic 2-20 Pure ß1-adrenergic effects Tachycardia
Tachyarrhythmias
Hypotension
Epinephrine Sympathomimetic 0.1-1.0 Adrenergic agonist effects, Tachyarrhythmias
predominately α1-adrenergic
Ventricular ectopy
effects
Hypertension
Myocardial ischemia
Milrinone Phosphodiesterase May use loading dose of Improves contractility Hypotension
enzyme inhibitor 50-75 µg/kg before infusion Afterload reduction
Thrombocytopenia
Ventricular ectopy
a α-adrenergic: constriction of veins and arteries; ß1-adrenergic: increased heart rate, contractility; ß2-adrenergic: vasodilatation, bronchodilatation.

treat poor cardiac contractility if trial32 is the only one in which output increase. Higher doses result
blood pressure is normal; in this researchers specifically looked at in stimulation of α1-adrenergic
instance, a purely inotropic agent is milrinone and improvement in car- receptors, causing further increase
recommended.26 diac function after myocardial injury; in heart rate and an increase in sys-
Milrinone, a phosphodiesterase thus, its results may be relevant to temic vascular resistance. Although
inhibitor, improves myocardial children with myocarditis. Milrinone initially blood pressure may increase,
diastolic function, resulting in is also less arrhythmogenic than cardiac output will ultimately
improved ventricular relaxation many other agents, making it the decrease. As heart rate increases,
and filling times. Although not inotropic agent of choice in many the myocardium loses filling time,
specific to myocarditis, improve- centers.24 and oxygen demand and consump-
ment in cardiac index and decreased Severe shock may require the tion markedly increase. With
systemic vascular resistance have addition of epinephrine, although increasing systemic vascular resist-
been reported in both pediatric and excessive administration of cate- ance, workload is amplified in an
neonatal populations with the use cholamines is discouraged. Epi- already failing myocardium. Epi-
of milrinone. The PRIMACORP nephrine is highly arrhythmogenic nephrine therefore is not routinely
study, a large, randomized, placebo- and markedly increases myocardial used as a first-line inotropic agent
controlled trial, showed the effec- oxygen consumption and workload.24 for myocarditis.33
tiveness of high-dose milrinone for Low doses (0.05-0.2 μg/kg per
preventing low cardiac output syn- minute) of epinephrine cause Arrhythmia Management
drome in children after cardiac sur- peripheral vasodilatation, increased Rhythm disturbances can be life
gery.32 Although postoperative cardiac heart rate, and improved contractil- threatening and must be treated
dysfunction differs from dysfunction ity. With adequate intravascular vol- aggressively. Ventricular ectopy,
related to viral myocarditis, this ume, stroke volume and cardiac ventricular tachycardias, and heart

50 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 http://ccn.aacnjournals.org

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019


Table 5 Intravenous antiarrhythmic agents

Drug Classification Dose Action Adverse effects


Adenosine Antiarrhythmic 0.05-0.1mg/kg rapid Slows conduction time through Arrhythmias
intravenous bolus the atrioventricular node,
Bradycardia
interrupting reentry pathways
Repeat to a maximum of
Heart block
0.3 mg/kg total
Hypotension
Can give 12 mg maximum
dose for children who
weigh >50 kg

Digoxin Cardiac glycoside See Table 6 Positive inotropic effects Sinus bradycardia
Decreases conduction Atrioventricular block, sinoatrial block
through the sinoatrial and
Ventricular arrhythmias
atrioventricular nodes
Hyperkalemia with toxic effects

Amiodarone Antiarrhythmic Loading: 1 mg/kg given Inhibits adrenergic stimulation Bradycardia, heart block, sinus arrest,
over 5-10 minutes, can paroxysmal ventricular tachycardia
be repeated 5 times
Continuous intravenous Decreases atrioventricular node Congestive heart failure, cardiogenic
infusion at 10-15 mg/kg conduction and sinus function shock, hypotension
per day
Pulmonary toxic effects (pneumonitis,
fibrosis, acute respiratory distress
syndrome)
Lidocaine Antiarrhythmic Loading: 1 mg/kg followed Suppresses automaticity of Bradycardia, heart block, arrhythmias,
by a continuous infusion the conduction system hypotension, seizures
of 20-50 µg/kg per
minute

block can develop in children with has improved survival rates after determined by resolution of
myocarditis.10-12,26 Adding to the chal- cardiac arrest due to ventricular ectopy and achieving an adequate
lenge of arrhythmia management is tachyarrhythmias. Thus, the Ameri- therapeutic serum concentration
determining whether the rhythm can Heart Association34 now recom- (1.5-5 μg/mL).
disturbance is the result of myocar- mends amiodarone as the first-line Although digoxin has led to
dial inflammation, hypoxia, inotropic antiarrhythmic therapy in pulseless improvement in patients with heart
therapy, or a combination of those ventricular tachycardia. Amiodarone failure, it is not routinely used dur-
factors (Table 5). requires a loading dose; in some ing the acute phase of myocarditis.
Regardless of the cause, tachy- patients, the ectopy stops after the Digoxin increases cytokine produc-
arrhythmias must be controlled to loading dose is administered. tion as well as intracellular calcium
prevent further deterioration of Other patients require a continu- loading, which, in patients with
ventricular function. For patients ous infusion. myocardial inflammation, can
with supraventricular tachycardia, Ventricular ectopy, unifocal or induce or worsen ventricular
adenosine is used for those whose multifocal, is common, as in K.M.’s arrhythmias. If digoxin is used, the
hemodynamic status is stable; case (see Figure 1). Ventricular ectopy loading dose should be no more
electrocardioversion is used for is often treated with lidocaine, the than 75% of the normal total load-
those whose hemodynamic status most widely used class IB antiar- ing dose24,35 (Table 6).
is unstable. rhythmic agent in pediatric critical If complete atrioventricular
In children with recurring supra- care.26 As with amiodarone, a load- block or second-degree block with
ventricular tachycardia, amiodarone ing dose is required, followed by a inadequate perfusion develops, a
has shown clinical effectiveness and continuous infusion. Dosing is temporary transvenous or epicardial

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 51


Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019
PediatricCare

pacemaker may be used. Insertion Anticoagulation at 13 years with high-dose cyclo-


of a permanent pacemaker is indi- Reports of the use of anticoagu- sporine (6-8 mg/kg per day; dose
cated if heart block persists for lants in patients with myocarditis adjustment when therapeutic serum
more than 2 weeks.11,26 are largely anecdotal, and such use levels were reached) and prednisone
is not supported by retrospective (2 mg/kg per day, tapered off over 6
Fluid Management studies of adults with heart failure.33 months). Ahdoot et al37 found sig-
The goal of fluid management is Severely compromised ventricular nificant improvement in left ventric-
to maintain an intravascular volume function and stasis of blood flow, as ular function in 5 patients with acute
sufficient to preserve preload and can occur in depressed myocardial viral myocarditis after combination
ventricular filling without overload.26 function, can increase the risk for treatment with muromonab (OKT3),
In acute or decompensated heart thrombus formation. Thrombi intravenous immune globulin, and
failure, diuretics are often adminis- potentially can embolize to the cere- high-dose methylprednisolone. In
tered because removal of excess brovascular system (causing neuro- that study, 4 patients also received
intravascular volume may help logical sequelae) or to the pulmonary cyclosporine, 3 received azathioprine,
improve cardiovascular function.24 vasculature. Because of the increased and 1 received a 2-month course of
Diuretics are administered cautiously risk for thrombus formation, use of methotrexate. Although Ahdoot et
because too rapid a removal of anticoagulation is common, typically al found improvement in function
intravascular fluid can result in done as a continuous infusion of with immunosuppressive therapy in
hypovolemia and hypotension. heparin in the critical care unit. a small sample, their study is skewed;
Tobias et al24 recommend initial Dosing varies depending on age, and 4 of 5 patients also received addi-
dosing of furosemide at 0.1 to 0.25 the dose is titrated to maintain a tional therapies.
mg/kg per dose to prevent an exces- predetermined anticoagulatory state. Although these studies indicate
sive reduction in cardiac output. that immunosuppression is safe in
Doses can be repeated every 6 to 12 Immunosuppressive Therapy children with myocarditis, without
hours up to 2 mg/kg per dose. Because immune dysfunction large, randomized controlled stud-
Furosemide can also be administered may play a primary role in many ies, it cannot be determined if out-
as a continuous infusion at 0.1 to cases of myocarditis, immunosup- come is worse without the addition
0.4 mg/kg per hour, with the addi- pressive therapies might shorten of immunosuppressive therapies.
tional benefits of maintaining a con- the course and lessen the severity of Currently no randomized controlled
stant serum level and minimizing illness. Intravenous immune globu- trials of immunosuppressive therapy
the opportunity for sodium retention lin is beneficial in the treatment of in children with myocarditis have
by the kidneys.24 Once the acute children with acute myocarditis.10,17 been done. Because children overall
episode of failure is controlled, other Improvement in left ventricular have higher recovery rates than adults
diuretic agents, including thiazides function and 1-year survival rate in for many diseases, the question is
(diuril) and spironolactone, are used. patients with biopsy-proven whether children with myocarditis,
myocarditis has with or without immunosuppression,
Table 6 Intravenous digoxin dosing been demon- intrinsically have a higher recovery
Digitalizing dose,a Maintenance dose,
strated after rate than adults do.10 Thus, the ben-
Age µg/kg µg/kg treatment with a eficial effects of immunosuppression
Full-term neonate 20-30 5-8 single, high dose in children with viral myocarditis
1 month to 2 years 30-50 7.5-12 of intravenous have yet to be determined.
2-5 years 25-35 6-9 immune globulin
5-10 years 15-30 4-8 (2 g/kg body Rescue Therapies
>10 years 2-3
weight).17 In chil- In children with progressing low
8-12
a Recommended dosing based on average patient response. Recommended
35
dren, Gagliardi et cardiac output syndrome, use of
dosing for children with myocarditis is 75% of the usual dose, with digitaliza- al36 reported an extracorporeal life support may be
24
tion accomplished over 24 to 36 hours.
83% survival rate necessary. Clinical guidelines for the

52 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 http://ccn.aacnjournals.org

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019


institution of extracorporeal life therapeutic effects of medication decrease the need for blood gas
support include escalating inotropic deliveries), prevention of complica- analyses.42
support associated with ongoing tions, and family support (Table 7). Once correct placement of the
metabolic acidosis and elevated endotracheal tube has been estab-
serum levels of lactate.38,39 ECMO Oxygenation, Ventilation, and lished, positioning and security of
and ventricular assist devices have Airway Management the tube should be routinely assessed.
been used in patients who do not Oxygen delivery should be Such assessment can be done by
respond to maximal conventional maximized. The method of delivery noting the centimeter mark where
management and as a bridge to trans- depends on the child’s signs and the tube is taped at least once a
plantation. Because of the physical symptoms and severity of illness. shift and ensuring that the tape is
limitations of ventricular assist Most children will require some secure. The depth of the endotra-
devices, ECMO should be consid- form of positive pressure ventilation cheal tube is noted on daily chest
ered for infants and small children. via nasal cannula or face mask. Posi- radiographs. The tip of the endotra-
Unfortunately, the long-term support tive pressure ventilation has shown cheal tube should be 1 to 2 cm
obtained with the use of ventricular benefit in patients with congestive above the carina or at the level of
assist devices has not been possible heart failure (improvement in gas T3. All attempts should be made to
with ECMO; most published case exchange, decreased work of breath- ensure neutral alignment of the
studies are limited to less than 2 ing, and afterload reduction of the patient’s head and neck when chest
weeks’ duration.40 left ventricle).33 Positive pressure radiographs are obtained. Depth of
In children who weigh more ventilation can be noninvasive in the endotracheal tube is altered
than 15 kg, ventricular assist devices the form of continuous positive air- with neck flexion, neck extension,
can offer long-term support with way pressure or bilevel positive air- and turning of the head.
excellent quality of life. In Europe, way pressure. Both of these types of Tracheal length varies markedly
pulsatile ventricular assist devices positive pressure ventilation are with age. Infants and small children
(Berlin Heart EXCOR, Berlin, Ger- associated with improvement in car- have short tracheas. Oral to carina
many; MEDOS VAD System, Stoberg, diac and respiratory functioning in lengths vary, from 12 to 14 cm in
Germany) have shown promise in patients with acute heart failure and newborns, 14 to 16 cm in 1- to 3-
children who weigh less than 15 kg can potentially postpone the need year-olds, 17 to 18 cm in 8- to 10-
and are as young as 2 days old.41 In for intubation. Long-term benefits year-olds, and 20 to 22 cm in 16-
the United States, pulsatile devices in children with viral myocarditis, year-olds.43 Because of the short tra-
for infants and small children are however, are unknown.33 More cheal length in small children, sim-
being developed.42,43 often than not, children who arrive ple turning of the head can cause
in the PICU with respiratory com- malalignment of the endotracheal
Nursing Considerations promise and low cardiac output tube or accidental extubation. Pre-
Care of children with suspected syndrome require intubation and venting flexion or extension of the
or proven viral myocarditis is chal- mechanical ventilation. head and neck is necessary not only
lenging. The responsibilities of pedi- Nursing care of intubated children when obtaining a chest radiograph
atric critical care nurses are numerous is focused on careful monitoring of but also when repositioning the
and include, but are not limited to, oxygenation and ventilation and patient. Flexion of the neck short-
airway management with adequate prevention of complications. Arte- ens the airway between the mouth
oxygenation and ventilation, detec- rial blood gases are typically assessed and carina, causing the endotracheal
tion and management of arrhythmias, on a routine basis; however, contin- tube to move downward, increasing
ongoing monitoring of hemody- uous monitoring of oxygen satura- the possibility of migration of the
namic parameters (including ade- tion and end-tidal carbon dioxide tube into the right main bronchus.
quacy of intravascular volume and levels are excellent noninvasive Findings would include an immedi-
tissue oxygenation), pain manage- means for determining the effective- ate increase in peak pressure (vol-
ment/comfort (including assessing ness of mechanical ventilation and ume ventilation) or a decrease in

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 53


Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019
PediatricCare

Table 7 Myocarditis: nursing considerations


Topic Nursing considerations
Airway Maintain patency of endotracheal tube
• Perform routine checks of tape security
• Note depth on daily chest radiograph (1-2 cm above carina or at T3)
• Maintain neutral head and neck alignment, particularly when repositioning and obtaining chest radiographs
• Reassess breath sounds after every position change
• Perform endotracheal suctioning on an as-needed basis only: increased airway pressure, decreased tidal volume,
decreased oxygen saturations, secretions in endotracheal tube, rhonchi, coughing
• Avoid instillation of normal saline with suctioning
• Use neuromuscular blockade in conjunction with sedatives if necessary
Oxygenation Monitor and maintain gas exchange
and ventilation • Continually monitor oxygen saturation, end-tidal carbon dioxide, arterial blood gases if applicable
Minimize oxygen demand/consumption
• Delay or cluster nursing interventions, depending on patient’s tolerance
• Maintain normothermia
• Minimize pain, anxiety
- Use nonsteroidals, opioids, anti-anxiolytics as needed
- Assess and eliminate any external, internal, or environmental factors contributing to anxiety
- Keep environment calm and quiet
Hemodynamic Be alert for ectopy, tachyarrhythmias, bradyarrhythmias, atrioventricular blocks
status • Differentiate between sinus tachycardia and supraventricular tachycardia (may need 12-lead electrocardiogram)
• Have adenosine (hemodynamically stable supraventricular tachycardia) and defibrillator (hemodynamically unstable
supraventricular tachycardia) available
• Administer, evaluate, and titrate antiarrhythmics
- Amiodarone, lidocaine
• Maintain pacemaker
- Transthoracic: ensure proper placement and adherence of electrode, change electrodes every 24 hours
- Transcutaneous: monitor for signs of cardiac tamponade, follow hospital’s policy for care of insertion site
- Keep extra battery at patient’s bedside
Monitor tissue perfusion
• Assess pulse quality, capillary refill, skin temperature and color, urine output, mental status if applicable
Continually monitor arterial blood pressure
• Be alert for fluctuations in blood pressure or hypotension
• Administer, evaluate, and titrate inotropic and/or vasoactive infusions
• Carefully assess extremity distal to arterial catheter for skin color, temperature, pulse, numbness, and tingling
Monitor central venous pressure
• Use distal port for monitoring if possible
• Monitor at least hourly, continuously preferred
• Assess for changes after delivery of fluid bolus and diuretic therapy
• Assess in context with entire clinical picture
- Recognize variables that affect central venous pressure: positive pressure ventilation, positive end-expiratory
pressure, conditions that increase peripheral vascular resistance, right ventricular dysfunction
• Monitor trends, not necessarily actual numbers
• Monitor for complications: bloodstream infection, thrombus, catheter occlusion
Prevention of Monitor for hospital-acquired infection
complications • Monitor body temperature at least hourly
• Assess white blood cell count, differential
• Assess for changes in pulmonary secretions: color, viscosity, amount
• Assess for changes in urine characteristics
• Assess catheter insertion sites for redness, edema, drainage
Prevent alterations in skin integrity
• Keep skin free from moisture and secretions
- Use moisture-barrier products
- Apply topical moisturizers (free from alcohol or perfume)
• Perform mouth care a minimum of every 8 hours
- Keep oral mucosa clean and moist
• Apply artificial tears, eye lubricant as needed
• Turn patient frequently and alleviate pressure points
- Use pillows, stuffed animals
- Use an air mattress or rotating bed
• Alternate position of mechanical devices (oxygen saturation probes, blood pressure cuffs, electrodes)
Continued

54 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 http://ccn.aacnjournals.org

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019


Table 7 Continued
Topic Nursing considerations
Comfort Routinely assess pain and/or agitation by using hospital-approved scales
Provide comfort measures
• Repositioning, calm, quiet environment, parents at bedside, elimination of factors potentially contributing to agitation
Administer opioids, nonsteroidals, sedatives as ordered
• Monitor for effectiveness after administration
Family support Recognize uniqueness of parental stress
• Alteration in parental role
• Loss of control
• Loss of ability to care for child
• Disruption of parent-child relationship
Use Nursing Mutual Participation Model of Care
• Individualize nursing interventions to fit parent and family
- Recognize and support parent-child connectedness
- Empower parents
Deliver concise, consistent information
Provide anticipatory guidance
Act as a role model
Encourage parental participation in care when appropriate
Encourage active parental involvement in child's daily plan of care

tidal volume (pressure ventilation), ated with complications, including necessary. Conversely, some or all
a decrease in oxygen saturation, and hypoxemia, bradycardia, atelectasis, of these activities may be clustered
asymmetric chest rise. If the tube and dysrhythmias. Suctioning should if tolerated in order to allow longer
migrates into the right main bronchus, be done on an as-needed basis rather periods of rest.
the child should immediately be than routinely. Indications for suc- Fever increases oxygen consump-
placed back in the previous position tioning include increase in airway tion 10% for each 1ºC elevation in
and reassessed. Breath sounds pressure, decrease in tidal volume, body temperature. Although not all
should be assessed after any change decrease in oxygen saturation, visu- fever is “bad,” treatment of fever is
in body position. alization of secretions in the tube, recommended in children with car-
Neck extension increases airway development of rhonchi, and cough- diopulmonary disease. Attempts
length, potentially causing uninten- ing. Hyperoxygenation may or may should be made to maintain nor-
tional extubation because the uncuffed not be required before suctioning, mothermia.26 Unless contraindicated,
tube can easily pass upward through depending on the child’s arterial antipyretics (acetaminophen,
the vocal cords. Immediate respiratory oxygenation and tolerance to the ibuprofen) should be administered.
distress, decrease in oxygen saturation, procedure. The catheter should not Fever reduction can also be attempted
marked decrease in or undetectable be deeper than the end of the endo- with external cooling, usually by
end-tidal carbon dioxide levels, grunt- tracheal tube. Catheters inserted to sponging with tepid water.
ing, or vocalization can indicate possi- the point of resistance (carina) cause Pain and anxiety significantly
ble inadvertent extubation. If tissue inflammation and damage.45 increase oxygen demand and con-
dislodgement of the endotracheal Instillation of normal saline for lavage sumption and cause considerable
tube into the esophagus is sus- should be avoided because that distress for children in the PICU.
pected, the tube should be removed practice is not supported by research Assessment and management of
and bag-valve-mask ventilation per- and may actually be harmful.44,45 pain and anxiety should be ongoing.
formed until reintubation or effec- Routine bedside nursing inter-
tive spontaneous breathing occurs. ventions such as dressing changes, Arrhythmias
Although a common practice in bathing, weighing, and reposition- Heart rate and rhythm require
intensive care units, endotracheal ing all significantly increase tissue monitoring. Arrhythmias are a sig-
suctioning should not be performed oxygen consumption. Delay in car- nificant life-threatening complica-
routinely.44 Suctioning can be associ- rying out these procedures may be tion of myocarditis.24 Development

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 55


Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019
PediatricCare

of bradycardia or tachyarrhythmias extra battery should be kept at the namic status or cardioversion in
is unlikely to be tolerated and requires bedside of any patient who is pace- patients with unstable hemodynamic
immediate recognition and treatment. maker dependent. Hospital policy status is performed. A defibrillator
Infants and small children depend should be followed when caring for should remain near any child who
on heart rate for adequate cardiac the insertion site and catheter. has myocarditis or recurring
output because stroke volume is Conversely, an excessively rapid supraventricular tachycardia.
relatively fixed; in young children, heart rate will decrease ventricular
bradycardia can rapidly diminish filling time, resulting in inadequate Hemodynamic Monitoring
cardiac output. Because chronotropic preload and subsequent cardiac With invasive hemodynamic
drugs can induce ventricular tachy- output. Tachycardias also result in monitoring, physiological variables
cardia in patients with viral inadequate coronary artery filling specific to cardiovascular function
myocarditis, cardiac pacing is the time. Coronary arteries fill and per- can be monitored and, when cou-
preferred treatment for life-threat- fuse the myocardium during diastole; pled with clinical examination, the
ening bradyarrhythmias, including the faster the heart rate, the shorter results provide data for sound clini-
atrioventricular block.25 is diastole, leading to a decrease in cal decision making.
Transcutaneous or transthoracic myocardial oxygen supply during a Arterial Pressure. Continuous
pacing is a noninvasive procedure time of increasing consumption. blood pressure monitoring via an
that can be done rapidly. Two elec- Differentiation between sinus arterial catheter is preferred in chil-
trodes are placed on the patient tachycardia and supraventricular dren with severe cardiac dysfunc-
with the anterior electrode in the V2 tachycardia is critical. Typically, tion, particularly those who require
to V5 position and the posterior sinus tachycardia is heart rate greater infusions of vasoactive agents. Non-
electrode under the scapula to the than 140/min in children, greater invasive measurements may be inac-
left of the spine. Electrode adher- than 160/min in infants, and varies curate or impossible to obtain
ence should be checked frequently, from beat to beat. Heart rate gener- because of impaired peripheral
especially if the child is diaphoretic. ally remains less than 200/min. perfusion and vasoconstriction.
If needed for prolonged periods, Sinus tachycardia can be the result Arterial catheters can be placed
electrodes should be changed a min- of a variety of factors, including peripherally (radial artery) or cen-
imum of every 24 hours to maintain fear, anxiety, fever, pain, intravas- trally (femoral artery) and provide
effectiveness of the contact gel. cular dehydration, and marked a dynamic picture of systolic, dias-
For ongoing bradyarrhythmias, vasodilatation. Sinus tachycardia tolic, and mean blood pressures.
invasive pacing should be considered. will resolve, or partially resolve, Because evaluations of interventions
Transvenous leads are placed percu- with resolution of the inciting factor. and their effectiveness will be based
taneously via a large vessel into the Supraventricular tachycardia is partly on invasive measurement of
right atrium or ventricle. Leads are an extremely rapid heart rate (200- blood pressure, care must be taken
stiff; nurses must be alert for indica- 280/min); is unresponsive to resolu- to ensure accuracy of readings. Rou-
tions of ventricular perforation, tion of fever, pain, hypovolemia, and tinely inspecting for proper trans-
including cardiac tamponade. An so on; and has no beat-to-beat vari- ducer placement (phlebostatic axis),
ability. Rates of sinus tachycardia zeroing the transducer a minimum
Sidebar and supraventricular tachycardia of once a shift, inspecting for and
can overlap, making determination eliminating air bubbles in the sys-
As a general rule, for children more
of the type of tachycardia difficult. tem, and using noncompliant pres-
than 1 year old, estimated systolic
blood pressure norms can be calculated A 12-lead electrocardiogram may be sure tubing will help ensure
as follows: necessary to differentiate between accurate measurements.
50th percentile = the two. Once supraventricular Normal blood pressure in chil-
90 mm Hg + (2 x age in years)
tachycardia has been established, dren is dependent on age and size27
5th percentile = rapid treatment with adenosine in (see Sidebar). As previously noted,
70 mm Hg + (2 x age in years)
the patients with stable hemody- however, children with myocarditis

56 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 http://ccn.aacnjournals.org

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019


can maintain a blood pressure these variables requires immediate tinuous intravenous administration
within normal limits for age until attention and potentially removal of fluids and/or drugs, CVP should
very late in the disease. No single of the catheter. be assessed a minimum of once an
clinical parameter should determine Central Venous Pressure. Central hour and after any administration
critical care interventions, and this venous pressure (CVP) or right atrial of fluid boluses or diuresis. When
rule is particularly true for blood monitoring provides a continual intermittent CVP monitoring is
pressure, unless hypotension is pres- reflection of intravascular volume used, care must be taken to ensure
ent. Adequacy of tissue perfusion is status and is a good determinant of that no cardiotonic medications are
determined by analysis of clinical right ventricular end-diastolic vol- infused through the distal port. If
findings on bedside examination ume, or preload. CVP should be such infusions are used, turning the
along with blood pressure. interpreted along with other meas- stopcock for pressure readings
The extremity distal to the arte- ures of cardiac function (heart rate, causes a disruption in the delivery
rial catheter should be assessed at peripheral perfusion, urine output). of medication and potential hemo-
least once a shift to monitor for any In critically ill children, the absolute dynamic compromise. Ideally, infu-
compromise in perfusion related to value is not as important as serial sions of inotropic or vasoactive
catheter placement. Extremity cool- measurements and changes in agents should be given through the
ness, color changes, delayed capillary response to interventions. medial or proximal lumen only.
refill, and diminishing pulse quality CVP monitoring should be done Normal CVP values can vary
can indicate inadequate perfusion. via the distal lumen of the catheter. widely in infants and children,
Numbness, tingling, and motor Monitoring can be continual or depending on age, disease, con-
deficit can also be indicators of intermittent, depending on avail- comitant conditions, and critical
impaired circulation. Development ability of intravenous access. If the care therapies. In healthy infants,
or change in any one or more of distal lumen is being used for con- normal values can range from -2 to

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019


PediatricCare

+4 mm Hg, from 4 to 8 mm Hg in intrathoracic pressure increases Complications of central venous


those with congenital heart disease, CVP. Values lower than expected catheters include bloodstream infec-
and from 2 to 6 mm Hg in those with may or may not indicate hypov- tion (increased risk with multilu-
respiratory disease requiring mechan- olemia; high CVP values may or men catheters), venous thrombosis,
ical ventilation. In this age group, may not indicate hypervolemia. Ele- thrombophlebitis, and catheter
measurements above 8 mm Hg are vated CVP values may also occur in occlusion. Routine maintenance of
generally indicative of myocardial patients receiving positive pressure the catheter and insertion site should
dysfunction or high intrathoracic ventilation and with the addition of be done per hospital policy.
pressure.46 In older children with- positive end-expiratory pressure. Pulmonary Artery Pressure. Pul-
out underlying disease, a CVP range Conditions that increase pul- monary artery catheters can provide
of 2 to 6 mm Hg is considered nor- monary vascular resistance valuable information in children
mal. Values can vary markedly and (hypothermia, hypoxemia, acidosis, with cardiopulmonary failure. The
should be interpreted along with severe respiratory disease, underly- ability to measure pulmonary artery
the child’s underlying disease state, ing pulmonary hypertension) also pressures, cardiac output/index,
concomitant conditions, and criti- increase CVP. High CVP values do and systemic and pulmonary vascu-
cal care therapies. not necessarily reflect cardiac dis- lar resistance can provide important
CVP measurements do not ease but may be an indication of data for directing therapies. How-
stand alone and must be consid- elevated right ventricular end-dias- ever, because of potential complica-
ered in context of the entire clinical tolic pressure, suggesting right ven- tions, pulmonary artery catheters
picture. Any changes in intratho- tricular dysfunction.26 Variables tend to be used less often in chil-
racic pressure will affect CVP val- that affect interpretation of CVP dren than in adults. Pulmonary
ues; spontaneous respirations values must be considered when artery catheters are therefore indi-
decrease CVP, whereas increased therapies are determined. cated only when the additional data

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019


obtained will enhance clinical deci- the most commonly used class of sedation and analgesia alone, oth-
sion making.26 analgesics. Children receiving opi- ers may require neuromuscular
oids should be monitored not only blockade to achieve synchrony. Neu-
Comfort for effectiveness of therapy but also romuscular blocking agents can be
Several pain intensity scales for for respiratory depression, particu- given intermittently or as a continu-
children are available; determining larly if they are dependent on spon- ous infusion. Before a chemical par-
which scale to use is based on the taneous breathing, with or without alytic agent is administered,
child’s age and/or ability to commu- mechanical ventilation. Hypotension patency of the airway and adequacy
nicate. Self-reporting scales can be can also occur after administration of sedation and analgesia must be
used with children who are able to of opioids. Dosing can be adjusted established. Neuromuscular block-
express their level of pain. The faces accordingly, or regimens can be ade should never be used without
scale is a visual scale that provides revised to minimize side effects. concomitant administration of an
facial expressions varying from no Acetaminophen, ketorolac, and opioid and/or an anxiolytic,
pain (smiling) to worst pain (deep ibuprofen (if not contraindicated) whether the paralytic agent is given
frown, crying). The child is asked to can be used for mild to moderate as a one-time dose or as a continu-
choose the facial expression that pain or as adjunct therapy in addi- ous infusion. Train-of-4 monitoring
best reflects his or her pain. The pain tion to opioids. should be routinely assessed for all
intensity scale is a numerical scale Anxiety in children is often children receiving continuous infu-
from 1 to 10, with 1 = no pain and expressed as agitation. Assessing sions of chemical paralytics, and
10 = severe pain. It is used with older agitation can be especially challeng- dosing should be titrated to the
children who understand the con- ing. Agitation is a means of commu- ordered level of neuromuscular
cept of rank and order. For infants, nicating physical and/or mental blockade.
scales designed for assessment of discomfort; many children in the
postoperative pain are available; PICU cannot communicate their Acquired Infection
these scales may or may not provide needs. Nurses must systematically Hospital-acquired infections are
adequate assessment of other types review and rule out any internal, a constant threat for any critically
of pain; thus subjective assessment external, or environmental factors ill child in the PICU. Acquired
by nurses within the context of the that may be causing or contributing nosocomial infection coupled with
clinical situation is critical. to agitation. extreme severity of illness in a child
In children who are unconscious, Anxiety and/or distress not with myocarditis significantly
are sedated, or require mechanical relieved with comfort measures (repo- increases morbidity and mortality.
ventilation, observational scales are sitioning the child, having a parent at Nurses’ diligence in preventing and
used. Unfortunately, these tools are the bedside, or quieting the environ- monitoring for infection is essential.
not effective for assessing pain in ment) are typically treated with seda- Within hours of admission,
children with chemically induced tives and anxiolytics (lorazepam, hospital-associated bacteria can be
paralysis because the tools require midazolam). These medications detected on skin and in the respira-
scoring of alertness and physical alleviate agitation and can provide tory and genitourinary tracts.45 Inva-
movement. For children with neuro- tolerance of invasive procedures and sive devices, antibiotic use, and/or
muscular blockade, bedside nurses intensive care therapies. Addition- critical care procedures increase the
must maintain a keen sense of ally, these medications provide a risk of bacterial invasion. Some of
awareness as to whether, given the lack of awareness, and subsequent the highest rates of hospital-
severity of illness and the treatments memory, of what can be an acquired infection occur in PICUs;
in use, it is reasonable to expect that extremely frightening experience. bloodstream infection and ventila-
a child is experiencing pain and, if The need for chemically induced tor-associated pneumonia are the
so, to treat the child accordingly. paralysis must be assessed on an indi- most common.45
For severe pain, opioids (mor- vidual basis. Although some children Fever is often the first sign of
phine, fentanyl, dilaudid) remain maintain ventilator synchrony with infection in children; however, infants

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 59


Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019
PediatricCare

often have decreases in body tem- bloodstream infections in the PICU.45 moisturizers, with avoidance of
perature because of the immaturity Unlike older children, young infants products containing perfume or
of the brain’s temperature-regulating commonly have neutropenia when alcohol, aids in maintaining skin
center. Monitoring of temperature infected because of their small stor- hydration. Mouth care, a minimum
changes in this age group can be age pools and inability to produce of every 8 hours, helps keep oral
complicated by the use of radiant white blood cells at a fast rate. mucosa clean and moist. In children
warmers, designed to maintain nor- Pulmonary secretions should be without a blink response (chemically
mothermia. Radiant warmer tem- monitored for changes in viscosity, paralyzed) or with incomplete lid
perature is adjusted according to an color, and amount. Changes in the closure, the eyes should be kept moist
infant’s skin temperature; conse- character of the secretions along with artificial tears and/or lubricant
quently, decreases in body tempera- with evidence of new pulmonary as needed. Frequent turning (as tol-
ture related to infection may be infiltrates may indicate the develop- erated), alleviation of pressure
masked. Although skin temperature ment of ventilator-associated pneu- points on bony prominences (use
is continuously monitored in infants monia (the second most common of pillows, stuffed animals), and
under a radiant warmer, core body hospital-acquired infection in PICUs) alternating pressure points related
temperature should be monitored a in intubated patients.45 Although to mechanical devices (oxygen satu-
minimum of once an hour, if not nosocomial urinary tract infections ration probes, blood pressure cuffs,
continuously, in all age groups. occur less often than do acquired electrodes) should be performed on
White blood cell count with a bloodstream or pulmonary infections a routine basis. Air mattresses or
differential count should be in children, urine should be rou- rotating beds can also be used to
assessed closely. Leukocytosis (ele- tinely examined for color, odor, and prevent skin breakdown. Any evi-
vation) or leukopenia (decrease) changes in opacity, particularly if a dence of altered skin integrity should
develop in children with infection, child has a urinary catheter in place. be immediately addressed.
depending on age. A normal total Any invasive catheter is a poten-
white blood cell count is 5000 to 10 tial source of infection. Insertion Family Support
000 cells/μL but varies depending sites should be routinely inspected As with all children admitted to
on the age of the child; the younger for edema, redness, and drainage. the PICU, the bedside nurse has an
the child, the higher the upper Although central venous catheters essential role in providing ongoing
range limit. Monitoring trends is as are not routinely changed in children, support and education to the
important as getting absolute counts. signs of infection at the site may war- patient’s family. Emergent admis-
The differential count provides rant removal of the catheter. Factors sion to the PICU creates feelings of
the percentage of each subset of increasing the risk for bloodstream overwhelming shock and disbelief
white blood cells (eosinophils, neu- infection include multilumen associated with helplessness.47,48
trophils, basophils, monocytes, and catheters, repeated catheterizations, The possibility of death is real and
lymphocytes) and can aid in differ- and certain types of dressing. In frightening. Adding to parental
entiating the type of infection. In order to minimize risk of infection, stress is alteration in the parental
older infants and children, a “shift catheters should be manipulated role, that is, loss of control and/or
to the left,” or an excess of imma- as little as possible and should be ability to care for their child. Alter-
ture neutrophils (bands), usually removed as soon as they are no ation in parenting and disruption
indicates bacterial infection. An longer needed. of the parent-child relationship are
increase in the number or percent- Immobility and alteration in tis- deemed the most stressful charac-
age of bands along with fever may sue perfusion increase the potential teristics of a PICU admission.47
warrant further workup (eg, blood for skin breakdown. Skin should be Use of the Nursing Mutual Partici-
cultures for detection of secondary kept free from exposure to moisture pation Model of Care can help nur-
bacterial infection). Coagulase- and secretions; moisture-barrier ture a trusting environment, establish
negative staphylococci are the most products can be applied to the per- effective communication patterns,
common cause of nosocomial ineal area. Application of topical and limit parental powerlessness.46

60 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 http://ccn.aacnjournals.org

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019


This model of nursing care focuses Prognosis For children with residual myo-
on the individuality of parental stress, The survival rate in children and cardial dysfunction at discharge,
recognizing that nurses’ perception adults with myocarditis is approxi- diuretics and afterload reducers are
of parental stress and actual parental mately 80%.46 Lee et al10 found that considered first-line agents. Diuretics
stress may differ greatly. Nursing patients who died almost always are used for congestive heart failure
interventions to alleviate stress must did so within the first few hospital of any cause because they reduce res-
be individualized to each family and, days. Survival after 72 hours in piratory signs and symptoms asso-
indeed, to individuals within the fam- patients not requiring ECMO is as ciated with heart failure.33 Thiazides
ily. Generic interventions, although high as 97%.10 Some centers have (diuril, hydrochlorothiazide) are often
well intended, may not be helpful. had a 1-year survival rate of 80% in used; the addition of spironolac-
Identification of individual coping children who required mechanical tone may obviate potassium supple-
mechanisms and appropriate nursing circulatory support.2 mentation. Angiotensin-converting
interventions are critical to enabling Unfortunately, survival to dis- enzyme inhibitors (captopril and
parental adjustment to the PICU.47 charge does not imply full recovery. enalapril) may also improve chronic
The Nursing Mutual Participa- Although Lee et al found that recov- signs and symptoms24 (Table 8).
tion Model of Care also recognizes ery of ventricular function without The use of digoxin in patients
and supports the value of parenting, the need for ongoing cardiac med- with chronic congestive heart fail-
parent-child connectedness, and the ications or restrictions in physical ure as a result of myocarditis remains
development of nurse-parent part- activity was the norm, some evi- controversial. The poor diastolic func-
nerships in caring for a critically ill dence suggests that myocarditis can tion associated with myocarditis is
child. Nurse-parent partnerships progress to dilated cardiomyopathy.10 not improved with digoxin.33 Digoxin
develop as nurses empower parents Viral persistence in the myocardium also increases the risk of ventricular
to maintain the parental role to the has been associated with progres- arrhythmias if myocardial inflamma-
fullest extent possible during a child’s sive impairment of left ventricular tion is still present. If digoxin is used,
critical care course. Such empower- function and is predictive of adverse digitalization should be accom-
ment is done in many ways, includ- outcomes.9,49 Progression from myo- plished during a 24- to 36-hour
ing (1) providing concise, consistent carditis to dilated cardiomyopathy is period with 75% of the usual total
information that enables parents to further supported by the finding of a loading dose to minimize the possi-
participate in decision making and coxsackievirus B–adenovirus receptor bility of arrhythmia development.24
daily goal setting; (2) role modeling gene present in larger amounts in the Beta-blockade may improve
activities traditionally done by nurses myocardium of patients with dilated outcome in children with dilated
but that parents can participate in cardiomyopathy than in healthy cardiomyopathy. Carvedilol, a non-
or lead; (3) providing anticipatory hearts.50 The discovery of this receptor selective β-blocker used in adults,
guidance to aid parents in distin- also suggests a role in not only the has been examined as an adjunct
guishing what is “expected” from viral origin of myocarditis but also therapy for management of heart
what is “unexpected” during the PICU the occasional “familial” case of myo- failure in children. Carvedilol may
course; and (4) providing options carditis.15 Survival in children with improve congestive heart failure
(step out or stay) during procedures dilated cardiomyopathy ranges through several mechanisms, includ-
and treatments. Parents of a criti- from 60% to 70% at 1 year to 34% ing decreased heart rate leading to
cally ill child are still parents; pro- to 56% at 5 years. Gagliardi et al36 improved myocardial oxygen con-
viding care supportive to their reported that in children with sumption and enhanced coronary
individual needs and enabling par- dilated cardiomyopathy, the first 2 artery blood flow, improvement in
enting activities will establish a ther- years after diagnosis are the most left ventricular ejection fraction,
apeutic nurse-parent relationship, in crucial.36 Favorable events (nearly and reduction in neurohormonal
the hope of making the experience complete recovery) and worse out- vasoconstrictor systems. Carvedilol
as a parent of a critically ill child as comes (death or need for a trans- may also prevent ventricular
positive an experience as possible.47 plant) occur during this period. arrhythmias and sudden death.

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 61


Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019
PediatricCare

Table 8 Angiotensin-converting enzyme inhibitors


than 10 days dial dysfunction. The most com-
and has no clini- mon techniques used in the PICU
Drug Dose Adverse effects cal signs of for children with cardiovascular
Captopril, oral Infants First dose: hypotension improvement.38 compromise or collapse include
0.15-0.3 mg/kg per Tachycardia invasive hemodynamic monitoring,
dose every 6-8 Conclusion infusions of inotropic agents,
Neutropenia
hours
Fever Viral myo- antiarrhythmics, afterload reduc-
Children
Hyperkalemia carditis ers, mechanical ventilation, pre-
0.3-0.5 mg/kg per
dose every 6-8 remains an vention of complications, and,
hours uncommon but when a child is unresponsive to
Enalapril, oral or 0.1 mg/kg per day First dose: hypotension challenging ill- ordinary PICU therapies, extracor-
intravenous divided into twice ness. In chil- poreal life support.
Fever
a day doses
Tachycardia dren, the initial
Maximum Financial Disclosures
0.5 mg/kg per day Neutropenia signs and None reported.
Hyperkalemia
symptoms are
often those of References
1. Aretz HT, Billingham ME, Edwards WD,
common pedi- et al. Myocarditis: a histopathologic defini-
tion and classification. Am J Cardiovasc
Use of carvedilol in children atric illnesses Pathol. 1987;1(1):3-14.
remains controversial. Bruns et al51 and without any obvious cardiac 2. Batra AS, Lewis AB. Acute myocarditis.
Curr Opin Pediatr. 2001;13(3):234-239.
studied the use of carvedilol in 46 signs. Adding to the challenge is 3. Leonard EG. Viral myocarditis. Pediatr
Infect Dis J. 2004;23(7):665-666.
children with heart failure in 6 dif- the potential inability of the child 4. Mecham N. Acute viral myocarditis in the
ferent centers and found improve- to convey precise symptoms or ED pediatric patient: three case presenta-
tions. J Emerg Nurs. 2004;30(2):179-182.
ment in left ventricular function describe location or intensity of 5. Levi D, Alejos J. Diagnosis and treatment of
pain or discomfort. A history of pediatric viral myocarditis. Curr Opin Car-
and overall signs and symptoms in diol. 2001;16:77-83.
67%. Schwartz and Wessel33 also asthma or congenital heart disease 6. Chavda KK, Dhuper S, Makhok A, Chowd-
jury D. Seizures secondary to a high-grade
examined use of carvedilol in chil- can skew the clinical picture. atrioventricular block as a presentation of
dren with heart failure and found Although few children actually acute myocarditis. Pediatr Emerg Care. 2004;
20(6):387-390.
no statistically significant effect; left have viral myocarditis diagnosed 7. Woodruff JF. Viral myocarditis. Am J Pathol.
1980;101(2):427-484.
ventricular ejection fraction and require admission to the PICU, 8. Feldman AM, McNamara D. Medical
improved in both the carvedilol and practitioners must maintain a progress: myocarditis. N Engl J Med. 2000;
343(19):1388-1398.
the placebo groups. Although heightened sense of awareness for 9. Calabrese F, Rigo E, Milanesi O, et al. Molec-
ular diagnosis of myocarditis and dilated car-
carvedilol is effective in reducing the “zebra in the herd of horses.” diomyopathy in children: clinicopathologic
mortality in adults, more research Concomitantly, for any previously features and prognostic implications. Diagn
Mol Pathol. 2002;11(4):212-221.
into the use of carvedilol is needed healthy child with sudden cardio- 10. Lee KJ, McCrindle BW, Bohn DJ, et al. Clini-
cal outcomes of acute myocarditis in child-
in children with heart failure. genic shock, myocarditis must be hood. Heart. 1999;82(2):226-233.
Transplantation is sometimes included in the differential diagnosis. 11. Friedman RA. Myocarditis. In: Garson A,
Bricher JT, McNamara DG, eds. The Science
the only option for children with Most children with myocarditis and Practice of Pediatric Cardiology. Philadel-
phia, PA: Lea & Febiger; 1990: 1577-1589.
significant cardiac failure or dilated recover without requiring admis- 12. Park MK, Troxler RG. Pediatric Cardiology
cardiomyopathy due to myocarditis. sion to the PICU; only a small per- for Practitioners. 4th ed. St Louis, MO:
Mosby; 2002:289-290.
Preferably, children are not put on a centage progress to development of 13. Martin AB, Webber S, Fricker FJ, et al. Con-
significant cardiopulmonary com- genital cardiovascular disease/diabetes:
list for transplantation until they acute myocarditis: rapid diagnosis by PCR
have progressed to the chronic phase promise that requires intensive car- in children. Circulation. 1994;90(1):330-
339.
of the disease, because recovery is diopulmonary support and 14. Baboonian C, McKenna W. Eradication of
possible in even the most severe monitoring. Critical care manage- viral myocarditis: is there hope? J Am Coll
Cardiol. 2003;42(3):473-476.
cases.2 Transplantation may, how- ment is aimed at supportive rather 15. Bowles NE, Towbin JA. Molecular aspects
of myocarditis. Curr Infect Dis Rep.
ever, be considered an option for a than curative measures and 2000;2(4):308-314.
child who requires ECMO for more depends on the severity of myocar- 16. Pres S, Lipkind RS. Acute myocarditis in

62 CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 http://ccn.aacnjournals.org

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019


infants: initial presentation. Clin Pediatr. congenital heart disease. Circulation. 49. Noutsias M, Fechner H, de Jonge H, et al.
1990;29(2):73-76. 2003;107(7):996-1002. Human coxsackie-adenovirus receptor is
17. Drucker NA, Colan SD, Lewis AB, et al. 33. Schwartz SM, Wessel DM. Medical cardio- colocalized with integrins αvβ3 and αvβ5
Gamma-globulin treatment of acute vascular support in acute viral myocarditis on the cardiomyocyte sarcolemma and
myocarditis in the pediatric population. in children. Pediatr Crit Care Med. 2006; upregulated in dilated cardiomyopathy.
Circulation. 1994;89(1):252-257. 7(6)(suppl):S12-S16. Circulation. 2001;104(3):275-280.
18. Kawai C. From myocarditis to cardiomyopa- 34. American Heart Association. 2006. 50. Noutsias M, Pauschinger M, Poller W,
thy: mechanisms of inflammation and cell http://www.americanheart.org. Accessed Schultheiss HP, Kuhl U. Immunomodulary
death. Circulation. 1999;99(8):1091-1100. November 15, 2007. treatment strategies in inflammatory car-
19. Kühl U, Pauschinger M, Noutsias, M, Kapp 35. Matsumori A, Igata H, Ono K, et al. High diomyopathy: current status and future per-
JF, Schultheiss HP. Diagnosis and treatment doses of digitalis increase the myocardial spectives. Expert Rev Cardiovasc Ther.
of patients with virus induced inflamma- production of proinflammatory cytokines 2004;2(1):37-51.
tory cardiomyopathy. Eur Heart J Suppl. and worsen myocardial injury in viral 51. Bruns LA, Christant MK, Lamour JM, et al.
2002;4(suppl I):I73-I80. myocarditis: a possible mechanism of digi- Carvedilol as therapy in pediatric heart fail-
20. Drucker NA, Newburger JW. Viral talis toxicity. Jpn Circ J. 1999;63(12):934- ure: an initial multicenter experience. J
myocarditis: diagnosis and management. 940. Pediatr. 2001;138(4):505-511.
Adv Pediatr. 1997;44:141-169. 36. Gagliardi MG, Bevilacqua M, Bassano C, et
21. Archard LC, Khan MA, Soteriou BA, Why al. Long-term follow-up of children with
HJ, Robinson NM, Richardson PJ. Charac- myocarditis treated by immunosuppression
terization of coxsackie B virus RNA in and of children with dilated cardiomyopa-
myocardium from patients with dilated car- thy. Heart. 2004;90(10):1167-1171.
diomyopathy by nucleotide sequencing of 37. Adhoot J, Galindo A, Alejos JC, et al. Use of
reverse transcription-nested polymerase OKT3 for acute myocarditis in infants and
chain reaction products. Hum Pathol. 1998; children. J Heart Lung Transplant. 2000;
29(6):578-584. 19(11):1118-1121.
22. Fujioka S, Kitaura Y, Ukimara A, et al. Eval- 38. Macrae D, Chang AC. Pediatric cardiac
uation of viral infection in the myocardium intensive care consensus: myocarditis.
of patients with idiopathic dilated cardio- Paper presented at: Pediatric Cardiac Inten-
myopathy. J Am Coll Cardiol. 2000;36(6): sive Care Symposium; December 11, 2005;
1920-1926. Miami, FL.
23. McCarthy RE, Boehmer JP, Hruban RH, et 39. Bohn D, Macrae D, Chang AC. Acute viral
al. Long-term outcome of fulminant myocarditis: mechanical circulatory support.
myocarditis as compared with acute (non- Pediatr Crit Care Med. 2006;7(6)(suppl):
fulminant) myocarditis. N Engl J Med. S21-S24.
2000;342(10):690-695. 40. Weiss WJ. Pulsatile pediatric ventricular
24. Tobias JD, Deshpande JK, Johns JA, Nichols assist devices. ASAIO J. 2005;51(5):540-545.
DG. Inflammatory heart disease. In: 41. Throckmorton AL, Lim DS, McCulloch
Nichols DG, Ungerleider RM, Spevak PJ, et MA, et al. Computational design and exper-
al, eds. 2nd ed. Critical Heart Disease in imental performance testing of an axial-
Infants and Children. Philadelphia, PA: flow pediatric ventricular assist device.
Mosby; 2006:899-925. ASAIO J. 2005;51(5):629-635.
25. Slota MC. Clinical assessment of cardiovas- 42. Yong ES, Timmons OD, Uhl MW, et al.
cular function. In: Slota MC, ed. Core Cur- Reduction of blood gases in a pediatric ICU
riculum for Pediatric Critical Care Nursing. (PICU): a process improvement. Paper pre-
2nd ed. Philadelphia, PA: WB Saunders Co; sented at: 11th Annual Pediatric Critical
2006:176-185. Care Colloquium; September 1998;
26. Craig J, Fineman LD, Moynihan P, Baker Chicago, IL.
AL. Cardiovascular critical care problems. 43. Thompson A. Pediatric emergency airway
In: Curley MAQ, Moloney-Harmon PA, eds. management. In: Dieckmann RA, Fiser
Critical Care Nursing of Infants and Children. DH, Selbst SM, eds. Illustrated Textbook of
2nd ed. Philadelphia, PA: WB Saunders Co; Pediatric Emergency and Critical Care Proce-
2001:629-631. dures. Louis, MO: Mosby-Yearbook Inc;
27. Hazinski MF. Children are different. In: 1997:104-115.
Hazinski MF. Nursing Care of the Critically 44. Curley MAQ, Thompson JE. Oxygenation
Ill Child. 2nd ed. St Louis, MO: Mosby; and ventilation. In: Curley MAQ, Moloney-
1992:1-17. Harmon, PA. Critical Care Nursing of Infants
28. Baughman KL. Diagnosis of myocarditis: and Children. 2nd ed. Philadelphia, PA: WB
death of Dallas criteria. Circulation. 2006; Saunders Co; 2001:233-308.
113(4):593-595. 45. Nguyen QV. Hospital-acquired infections.
29. Pophal SG, Sigfusson G, Booth KL, et al. http://www.emedicine.com/ped/topic1619
Complications of endomyocardial biopsy in .htm. Updated August 21, 2007. Accessed
children. J Am Coll Cardiol. 1999;34(7): November 27, 2007.
2105-2110. 46. Hastings LA, Heitmiller ES, Nyhan D. Peri-
30. Akhtar N, Ni J, Stromberg D, Rosenthal GL, operative monitoring. In: Nichols DG,
Bowles NE, Towbin JA. Tracheal aspirate as Ungerleider RM, Spevak PJ, et al. Critical
a substrate for polymerase chain reaction Heart Disease in Infants and Children. 2nd
detection of viral genome in childhood ed. Philadelphia, PA: Mosby; 2006:479-506.
pneumonia and myocarditis. Circulation. 47. Curley MAQ, Meyer EC. Caring practices:
1999;99(15):2011-2018. the impact of the critical care experience on
31. Lauer B, Neiderau C, Kuhl U, et al. Cardiac the family. In: Curley MAQ, Moloney-
troponin T in patients with clinically sus- Harmon PA. Critical Care Nursing of Infants
pected myocarditis. J Am Coll Cardiol. and Children. 2nd ed. Philadelphia, PA: WB
1997;30(5):1354-1359. Saunders Co; 2001:47-67.
32. Hoffman TM, Wernovsky G, Atz AM, et al. 48. Rothstein P. Psychological stress in fami-
Efficacy and safety of milrinone in prevent- lies of children in the pediatric intensive
ing low cardiac output syndrome in infants care unit. Pediatr Clin North Am. 1980;
and children after corrective surgery for 27(3):613-620.

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 1, FEBRUARY 2008 63


Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019
CE Test Test ID C0812: Viral Myocarditis in Children
Learning objectives: 1. Identify which population is at most risk of death as the result of myocarditis 2. Identify the mechanism that results in morbidity and
mortality in children with myocarditis 3. Discuss the signs and symptoms of myocarditits in children 4. Describe the treatment of patients with myocarditis
1. The mortality rate in infants with myocarditis can be as high as what 7. Which of the following statements is true for children with myocarditis?
percentage? a. Hypotension is an early sign of myocarditis.
a. 25% b. Hypotension is always present with myocarditis.
b. 50% c. Hypotension is extremely rare with myocarditis.
c. 75% d. Hypotension is a late and ominous sign.
d. 95%
8. Which of the following are common rhythm issues in children with
2. The incidence of myocarditis is more prevalent in which of the following? myocarditis?
a. Infants and adolescents a. Supraventricular tachycardia and premature ventricular contractions
b. Infants and toddlers b. Bradycardia with AV blocks
c. Infants and young adults c. Bradycardia with ventricular tachycardia
d. Adolescents and young adults d. None of the above

3. Which of the following plays a lead role in myocyte injury in patients 9. Which of the following disease processes may mimic myocarditis?
with myocarditis? a. Structural cardiac defects
a. The fever associated with the infection b. Pericardial effusion
b. The autoimmune reaction c. Pleural effusion
c. The exaggerated healing process forms scar tissue within the myocyte d. A and B
d. None of the above
10. How does dobutamine primarily work in the treatment of
4. Viral myocarditis (coxsackie B) predominately occurs in what population? hemodynamic compromise in children with myocarditis?
a. Men a. Decreasing contractility and increasing systemic vascular resistance
b. Women b. Increasing contractility and decreasing systemic vascular resistance
c. Both men and women equally c. Increasing contractility and increasing systemic vascular resistance
d. In women as adults and in men as children d. Decreasing contractility and decreasing systemic vascular resistance

5. Which of the following types of myocarditis results in worse outcomes? 11. How does milrinone primarily work in the treatment of hemodynamic
a. Chronic compromise in children with myocarditis?
b. Acute a. Decreasing systemic vascular resistance and increasing systolic function
c. Fulminant b. Increasing systemic vascular resistance and decreasing systolic function
d. Latent c. Increasing myocardial systolic function
d. Increases myocardial diastolic function
6. Which of the following characterize the signs and symptoms of
myocarditis in children? 12. Endotracheal suctioning should not be performed routinely due to
a. Easy to recognize and easy confirm diagnose which of the following?
b. Easy to recognize and hard to confirm diagnose a. The increased association with bradycardia and atelectasis
c. Hard to recognize and hard to confirm diagnosis b. The increased incidence of accidental extubation
d. Hard to recognize and challenging to confirm diagnosis c. The increased association with dysrhythmias and tachycardia
d. None of the above—routine suctioning is a good thing

Test answers: Mark only one box for your answer to each question. You may photocopy this form.
1. K a 2. K a 3. K a 4. K a 5. K a 6. K a 7. K a 8. K a 9. K a 10. K a 11. K a 12. K a
Kb Kb Kb Kb Kb Kb Kb Kb Kb Kb Kb Kb
Kc Kc Kc Kc Kc Kc Kc Kc Kc Kc Kc Kc
Kd Kd Kd Kd Kd Kd Kd Kd Kd Kd Kd Kd
Test ID: C0812 Form expires: February 1, 2010 Contact hours: 1.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%) Category: A, Synergy
CERP A Test writer: Katie Schatz, RN, MSN, APRN
Program evaluation Name Member #
Yes No
Objective 1 was met K K Address
Objective 2 was met K K
Objective 3 was met K K City State ZIP
Objective 4 was met K K
Country Phone
For faster processing, take Content was relevant to my
this CE test online at nursing practice K K E-mail
My expectations were met K K
http://ccn.aacnjournals.org This method of CE is effective RN Lic. 1/St RN Lic. 2/St
(“CE Articles in this issue”) for this content K K
Payment by: K Visa K M/C K AMEX K Discover K Check
or mail this entire page to: The level of difficulty of this test was:
AACN, 101 Columbia K easy K medium K difficult Card # Expiration Date
To complete this program,
Aliso Viejo, CA 92656. it took me hours/minutes. Signature
The American Association of Critical-Care Nurses is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation.
AACN has been approved as a provider of continuing education in nursing by the State Boards of Nursing of Alabama (#ABNP0062), California (#01036), and Louisiana (#ABN12). AACN
programming meets the standards for most other states requiring mandatory continuing education credit for relicensure.

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019


Viral Myocarditis in Children
Tammy L. Uhl
Crit Care Nurse 2008;28 42-63
Copyright © 2008 by the American Association of Critical-Care Nurses
Published online http://ccn.aacnjournals.org/
Personal use only. For copyright permission information:
http://ccn.aacnjournals.org/cgi/external_ref?link_type=PERMISSIONDIRECT

Subscription Information
http://ccn.aacnjournals.org/subscriptions/
Information for authors
http://ccn.aacnjournals.org/misc/ifora.xhtml

Submit a manuscript
http://www.editorialmanager.com/ccn

Email alerts
http://ccn.aacnjournals.org/subscriptions/etoc.xhtml

Critical Care Nurse is an official peer-reviewed journal of the American Association of Critical-Care Nurses (AACN) published
bimonthly by AACN, 101 Columbia, Aliso Viejo, CA 92656. Telephone: (800) 899-1712, (949) 362-2050, ext. 532. Fax: (949)
362-2049. Copyright ©2016 by AACN. All rights reserved.

Downloaded from http://ccn.aacnjournals.org/ by AACN on May 27, 2019

Das könnte Ihnen auch gefallen