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Course: Heart Assessment

Unit Title: Infants and Children

Jackie Christianson, MSN, RN, FNP-C

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Module Goals

Learner Outcome:

At the completion of these modules the learner will demonstrate knowledge and skills to perform a complete health assessment of an individual

Module Objectives:

Explain the changes that occur in circulation at birth and the need to repeat the cardiac assessment after 48 hours
Differentiate between normal and abnormal assessment findings with respect to the heart rate and skin color
Explain the importance of early identification of Rheumatic Fever in early childhood

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Fetal Circulation Review

Dependent on maternal circulation

No maternal circulation, no fetal circulation
Becomes more independent over time
Connected via umbilical cord
Not fully mature at birth – transition period after birth

Fetal circulation volume and shunting through the DV and FO varies depending on embryonic stage

Responsive to maternal conditions
Changes based on fetal development stage

Fetal circulation relies on several ducts that are not normally present in children and adults

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The fetal heartbeat is visible on ultrasound very early in development, before 10 weeks gestational age. The heart is the first functional organ that develops. Chambers and ability to pump some blood begins at approximately 5-6 weeks gestation but continues to develop until birth. The stroke volume of the heart is inadequate to fully perfuse the fetus and the fetus is dependent upon the mother for nutrients, so an alteration in maternal circulation can cause severe alterations in fetal circulations. Research shows even fairly minor fluctuations in maternal oxygen capacity, acidosis, and other pathologic changes in maternal circulation can have an impact on how the fetal circulation develops and shunts blood.

There is a transition period between fetal circulation and neonatal circulation that takes place, which we will discuss in another slide.

Fetal circulation volume and where the blood is shunted toward varies greatly during pregnancy. At week 28-32, fairly little blood is shunted through the ductus venosus and the foramen ovale is greatly reduced and the blood flow through the lungs is maximized; this time frame correlates to a very important time in lung tissue development. Some very recent obstetric studies suggest that the age of human functional fetal maturity (not age at which the infant is born!) may be approximately 32 weeks as determined in part by lung maturity.

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Fetal Circulation

Umbilical vein to inferior vena cava
Hole between right and left atrium – bypasses RV
Ductus arteriosus – connects pulmonary arteries to aorta
Umbilical arteries return blood to placenta
Portal sinus – additional blood flow to liver from placenta

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Remember: Vein is the term used for a blood vessel that takes blood toward the heart, artery is the term for a blood vessel that carries it away from the heart. The veins and arteries in this diagram refer to the fetus’ heart, not the mother’s. Therefore, the umbilical vein carries nutrient rich blood from the mother’s placenta (which is routed toward the infant’s heart) and the umbilical arteries take less oxygenated blood away from the infant’s heart back to the placenta. There are two arteries and one vein in the umbilical cord connecting the infant’s circulation to the placenta.

The umbilical vein attaches to the infant’s inferior vena cava. There is a duct between the umbilical vein and the vena cava called the ductus venosus that allows much of the blood in the umbilical vein to bypass the portal vein, delivering fresh nutrients almost directly to the heart. Some of the blood from the placenta does, however, go directly to the liver.

The inferior vena cava, supplied with nutrient-rich blood from the umbilical vein, enters the right atrium as it does in an adult. In the fetus, there is ordinarily a hole in the heart between the atria which is necessary for normal fetal circulation. Some of the blood does get diverted into the right ventricle, but most of the blood flow goes through the hole in the atrial septum into the left atrium (foramen ovale). From there, it is pumped by the fetus’ heart into the left ventricle and into general circulation.

The foramen ovale is a hole in the septum separating the atria. It is often referred to as a flap, and it normally closes shortly after birth in response to increased blood pressure. Increased pressure on the left side of the heart pushes the flap closed, where it eventually fuses closed.

The right ventricle does pump blood to the lungs as in an adult, but there is an additional difference in fetal circulatory structures called the ductus arteriosus. This duct connects the pulmonary arteries to the aorta, which allows some of the blood pumped by the right ventricle to enter general circulation and bypass the lungs. The lungs, however, do get some blood flow. The ductus arteriosus varies in diameter and capacity throughout fetal development; as mentioned earlier, the ductus arteriosus does constrict somewhat during weeks 28-32 to promote more blood flow to the lungs through the pulmonary arteries. The ductus arteriosus does remain open until birth and usually closes within the first few days after birth. The ductus arteriosus is very important to remember when discussing both congenital heart diseases. Some congenital defects of the heart are not compatible with life after the ductus arteriosus closes and it can be kept artificially open using medications.

The aorta supplies oxygenated blood to the rest of the fetus’ body as it does for an adult. The primary difference is the umbilical arteries that return blood to the mother via the placenta. The bilateral iliac arteries have ducts that branch off and form the umbilical arteries.

Fetal circulation is complex appearing and can be intimidating, but it is important to understand the differences to better understand heart assessment in children as well as the most commonly occurring congenital heart defects and how they are treated.

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Fetus to Infant Transition

First breaths prompt physiologic changes
Increased systemic blood pressure, decreased pulmonary blood pressure (placenta no longer feeding pulmonary vessels, pressure of air in lungs pushes back against pulmonary vasculature)
Closure of foramen ovale

Occurs very shortly after birth in most cases
Referred to as either patent foramen ovale or atrial septal defect when still intact after birth

Closure of the ductus arteriosus 24-48 hr after birth
Sphincter controlling duct tightens, eventually sealing

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Patient History

Reason for assessment

Routine visit vs illness

Reliance on caregiver

Okay to ask child question if appropriate
Family history: sudden cardiac death

History and behaviors

History known heart or lung problem
Fatigues easily, poor exercise capacity
Difficulty feeding, poor growth
Edema
Chronic cough
Complaints of pain, syncope or near syncope

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Pediatric Assessment Triangle

Valuable assessment tool for children
Useful in heart assessment
Circulation:

Pulse
Rate
Quality

Blood pressure
Skin quality and condition

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The pediatric assessment triangle is a very helpful assessment in evaluating children. It consists of 3 parts: appearance, work of breathing, and circulation. Today’s focus will be on circulation as part of your heart assessment.

The circulation assessment includes the pulse rate as a numeric value and its quality. Quality refers to what the palpable pulse feels like: is it strong, bounding, weak, thread, difficult to obtain peripherally, absent peripherally? Blood pressure can be helpful in assessing the child’s circulatory status, but in an ill child blood pressure is often one of the last vital signs to become abnormal and is a late indicator of a problem.

Skin quality and condition is an extremely important assessment to make in children and is part of the circulatory aspect of the pediatric assessment triangle. This will be discussed in more detail in another slide.

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Vital Signs in Infants and Children

Gradually normalize to adult VS normal range
Crying vs content vs asleep
HR and respirations very important when assessing illness severity

Abnormal VS in children should not be ignored
Ill children can compensate for illness via VS

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Vital signs in children are very different from those in adults, but you may notice that they start out very abnormal but normalize over time to the adult range. A heart rate of 160 in an adult is very high; a heart rate of 160 in an infant is normal. Using the heart rate as an example, you will notice that the normal range gradually decreases to the normal adult heart rate of about 60-90 by age 12. Vital sign normal ranges vary somewhat between sources, and it takes some practice to remember what the general ranges are between age groups.

You will notice a difference in vital signs if the patient is asleep, awake, and crying. Pulse, respirations, and BP tend to be lower when asleep, somewhat higher when awake, and can be considerably higher when crying, upset, or very active. Fever can also make the heart rate abnormally high.

Heart rate and respiratory rate are very important markers for pediatric patients. These two vital signs in particular can provide very valuable insight as to how ill a sick child is. A 4 year old child who outwardly appears well but has a heart rate of 170 without a fever and while at rest necessitates further investigation because of the heart rate alone. Children tend to compensate for critical illness very well through increased heart and respiratory rates, and this is often the first warning sign for serious illness. It is important to get an accurate measure of the patient’s pulse and respiratory rate for this reason; children also tend to lose their ability to compensate for illness fairly suddenly and seemingly without warning. Pediatric illnesses can be predicted in this nature, but vital signs are of vital importance in assessing the overall well being of a pediatric patient.

A good rule of thumb for a normal blood pressure is Age * 2 + 80. So a 2 year old child would have a normal SBP of approximately 84.

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Heart Assessment

Same assessment locations as adult

Aortic, pulmonic, tricuspid, mitral
Louder heart sounds are normal
Erb’s point not necessary in pediatrics

Bell vs diaphragm of stethoscope

Palpation of apical heart rate

4^th intercostal space
Slightly lateral to the mid-clavicular line

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A child normally has louder heart sounds than an adult because their chest wall is thinner and the heart takes up more space in the chest cavity compared to an adult. The x-rays visible on the slide shows a child on top, an adult on the bottom: notice how much larger the heart is in the child, extending well past the right mediastinal border. The heart sounds are often audible from the posterior as well as the anterior though the heart should be assessed from the anterior chest wall.

Heart sounds should be auscultated with both the bell and the diaphragm in pediatrics. The bell picks up higher pitched sounds than the diaphragm, which can be helpful in diagnosing heart murmurs that are very faint or soft.

The apical pulse can be palpated at the 4^th intercostal space, just lateral to the mid-clavicular line. This is helpful to know particularly when evaluating heart murmurs, as heart murmurs are graded based on both sound and if the murmur is also palpable.

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Heart Murmurs

Same are benign

Physiologic murmur
Seven S’s: Sensitive, short, single, small, soft, sweet, systolic

Murmur grading

Grade	Auscultation	Palpation
I	Barely audible	Not palpable
II	Soft, audible	Not palpable
III	Easily audible	Not palpable
IV	Easily audible	Palpable thrill
V	Loud; audible with only light stethoscope contact on chest	Palpable thrill
VI	Very loud; audible without direct stethoscope contact on chest	Palpable thrill

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Some heart murmurs are considered benign. A neonate that is <48 hours old, for example, is likely to have a low grade heart murmur due to a patent ductus arteriosus. An easy mnemonic to help remember how to differentiate a likely benign heart murmur from a pathologic one is the 7 S’s:

Sensitive: The murmur sounds different when the child is in different positions (standing vs sitting vs laying down)

Short: The duration of the murmur is short

Single: The murmur presents by itself, there are no clicks, friction rubs, gallops, or extra heart sounds associated with the murmur

Small: The murmur is only audible over a small area of the heart and does not resonate in all 4 auscultation points

Soft: The murmur is grade II or less

Sweet: The murmur does not sound harsh or machine-like

Systolic: The murmur occurs during systole

Murmurs are graded on a I-VI scale

Grade I through III are associated with sound only. A grade I murmur is barely audible. A grade II murmur is soft, but audible. A grade III murmur is easily audible but not palpable. A grade IV murmur is palpable and associated with a palpable thrill when palpating the apical pulse. A grade V murmur is loud, has a palpable thrill, and is easily audible even if the stethoscope is barely resting on the chest wall. A grade VI murmur is very loud and can be heard with the stethoscope near but not on the chest and has a palpable thrill.

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Newborn Heart Assessment

Murmur in newborn

1% of newborns have murmur that persists >48 hours after birth
Examination combined with pulse oximetry has 77% sensitivity for detecting congenital heart disease

Needs provider referral if persistent for >48 hours
Needs urgent provider referral if present at any time concurrently with other concerns

Hypoxia
Signs of heart failure
Dyspnea
Poor eating, failure to thrive

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Skin Assessment

Skin is an excellent indicator of overall circulation in children
Color

Appropriate for skin tone, cyanotic, erythematous

Turgor

How quickly does pinched skin spring back into place?

Condition

Is the skin thin, transparent, thick, visible scars?

Fingernails

Clubbing, discoloration of nail beds

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Congenital Heart Diseases

Nursing assessment alone inadequate to diagnose
Left shunting vs Right shunting defects

Also called cyanotic vs acynotic
Left side of heart is stronger than right

Right-to-left shunting defects

De-oxygenated blood flows into circulation without going to lungs
Cyanotic defects

Left-to-right shunting defects

Oxygenated blood flows back into the right chambers, returning unnecessarily to the heart
Non-cyanotic defects

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Congenital heart diseases are impossible to diagnosis with assessment alone, but a nursing assessment is a vital component of identifying congenital heart diseases. There are several kinds of congenital heart diseases: two types are referred to as either right-to-left shunting or left-to-right shunting defects. These are sometimes called cyanotic (right-to-left) or non-cyanotic (left-to-right) defects. These terms refer to where blood abnormally flows.

A left-to-right shunting defect is the opposite problem; it refers to a problem in which oxygen-rich blood from the left side of the heart is shunted abnormally into the right side of the heart. This does not cause cyanosis because de-oxygenated blood is not flowing into circulation, so these disorders are non-cyanotic, but these types of disorders tend to cause cause congestive heart failure-like features because blood is continuing to return to the right atrium via the vena cava, but it is also flowing back in abnormally from the left side of the heart leading to problems like fluid overload and pulmonary hypertension. Left-to-right shunts include ventricular septal defects (hole between the ventricles), atrial septal defect (hole between the atria), as the musculature on the left side of the heart tends to be larger and more powerful than the right side blood gets pushed more forecefully from the left side and therefore shunts abnormally into the right. A patent ductus arterosus is also considered a left-to-right shunt, as blood tends to flow out of the highly pressurized aorta into the less pressurized pulmonary vein.

A right-to-left shunting defect means the defect is causing shunting of the blood in the right side of the heart (which is oxygen-poor) to flow into the left side of the heart or the general circulation. This is a cyanotic heart defect because it infiltrates the ordinarily oxygen-rich blood going through the aorta into the peripheral circulation, decreasing how much oxygen is in the peripheral circulation and often causing visible cyanosis in the child. Examples of these disorders include tetralogy of fallot (combination of VSD and pulmonary stenosis; due to the pulmonary stenosis not much blood is able to flow into the pulmonary vein, and is instead shunted from the right to the left through the VSD as the aorta is still open) and pulmonary atresia (absence of pulmonary valve opening; blood is forced to flow from the right chambers through either an ASD or a VSD into the left chambers, this condition is not compatible with life unless the ductus arterosus is kept open).

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Congenital Heart Defects

Disorders that rely upon maintenance of the ductus arteriosus:
Cardiac obstructions

Right obstruction
Left obstruction

Abnormal vessel connections

Switching of blood vessel connection points
Abnormal fusion of blood vessels

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This slide discusses the classes of congenital heart defects that are reliant on the ductus arteriosus. While not all of the disorders mentioned on this slide require a patent ductus arteriosus to be compatible with life, some disorders are not compatible with life at all without a patent ductus arteriosus even with the most sophisticated medical technology available.

Cardiac obstruction diseases range in severity. They consist of stenosis of the arteries of the heart and hypoplasia (or under-development) of heart chambers. Not all cardiac obstructions are dependent upon the ductus arteriosus. Right sided obstructions include hypoplastic right heart syndrome, pulmonic stenosis, and tricuspid stenosis. They reduce the right side of the heart’s stroke volume, which causes symptoms consistent with right sided heart failure (ie: peripheral edema, hypertrophy of the liver, etc.). Left sided obstructions include hypoplastic left heart syndrome and coarcation of the aorta. They reduce the left side of the heart’s stroke volume, which causes symptoms consistent with left sided heart failure (ie: pulmonary hypertension and edema).

Disorders causing abnormal switching and fusion of blood vessels can cause severe illness in affected infants. These disorders are both cyanotic and usually fatal if not surgically corrected. The most common disorders, transposition of the great arteries and truncus arteriosus are usually not compatible with life when not surgically repaired; TGA is not compatible with life at all if the ductus arteriosus is allowed to close. There are also some very rare disorders called pulmonary inlet errors in which the pulmonary veins (which remember contain oxygenated blood) connect directly with the aorta and not with the left atrium that are generally not life-threatening. Some surgical procedures used to repair certain other congenital defects surgically create a direct connection between the pulmonary veins and the aorta intentionally to divert around a defective heart chamber.

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Signs of Pediatric Heart Failure

Similarities to adult heart failure

Systolic vs diastolic, left vs right
Signs of fluid overload similar

Differences in presentation

Poor growth, feeding difficulties, diaphoresis
Exercise intolerance, tachypnea at rest, central cyanosis
Pulses and blood pressures significantly different in different limbs
Hepatomegaly

Different causes compared to adults

Most often congenital heart disease
Sometimes cardiomyopathy, rarely CAD as in adults

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Rheumatic Heart Disease

Leading cause of acquired heart disease in the developing world
Inflammatory disease resulting in scarring of the heart tissue
Can cause short-term death
Can cause long-term disability
100% preventable
Extremely rare in Europe and North America

Acute cases are very rare
Chronic cases usually immigrants

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Acute Rheumatic Fever

Prodrome: group A strep infection

Ages 5-15, pregnant women
Sore throat, fever, chills, n/v, cervical lymphadenopathy
GAS impetigo common in tropical countries
CENTOR criteria screening tool
Occurs 2-4 weeks before ARF onset

Unclear specific trigger for immune response

Socio-economic aspects
Decline in ARF historically occurred before antibiotics

Treatment of GAS vs supportive care

European model
American model

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Acute rheumatic fever is an abnormal autoimmune response to a group A beta hemolytic streptococcus infection. This infection is most commonly either strep pharyngitis or, in tropical areas of the world, group A strep impetigo.

The CENTOR criteria is a clinical tool that may be used when screening for strep pharyngitis. It is a 5 question screening tool that is helpful, but not absolute when considering a throat swab for strep pharyngitis or treating empirically for strep. It is the following score:

Age: 3-14 years 1 point, 15-44 years 0 points, >45 years -1 point

Exudate or swelling on tonsils: If yes, 1 point

Tender/swollen cervical lymph nodes: If yes, 1 point

Temp >38C or 100.4F: If yes, 1 point

Cough: If yes, -1 point

The maximum score is 4. For scores of 1 or less, no testing or antibiotics is required. For scores of 2, testing is optional. For scores of 3-4, there is a 28-53% probability of GAS infection; while empiric treatment is no longer officially recommended it may be considered if testing is not available.

The trigger that causes acute rheumatic fever is unclear; there is a definite link to GAS, but the specific link mechanisms are unclear. In the United States, it is routine practice to treat all confirmed GAS infections with an antibiotic to prevent ARF. In Europe, it is not necessarily routine practice to treat all GAS with antibiotics and symptom management is usually recommended. The rates of ARF similar in the US and Europe, but higher in areas like Africa and Southeast Asia. Additionally, ARF rates historically started to decline during the Industrial Revolution before the first antibiotics were developed. It is therefore theorized that there is a socio-economic, hygiene, or living condition-related element in development of ARF. Treatment of GAS within 7 days of onset, however, is associated with a near-eradicaiton of ARF and is therefore the recommendation for patients in the developing world with GAS.

The primary age group affected by ARF is children ages 5-15. This is also the group most affected by GAS infections; rates decline significantly after age 15 and are fairly uncommon in adults over age 30. The risk for pregnant women roughly doubles compared to their non-pregnant counterparts.

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Acute Rheumatic Fever Diagnosis

Jones criteria for diagnosis

First time exacerbation

One major criteria, two minor criteria
Two major criteria

Recurrence of ARF

Same as first time, additionally three minor criteria

Major Criteria	Minor Criteria
Carditis	Prolonged PRI on ECG
Migratory joint pain, swelling	Arthralgias
Chorea	Fever >38C or >100.4F
Erythema marginatum	ESR >60
Subcutaneous nodules	CRP >3

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The Jones criteria is the most widely used clinical criteria for acute rheumatic fever diagnosis. It requires documentation of a recent streptococcal infection concurrent with at least either two major criteria or one major and two minor criteria.

Of particular concern in acute rheumatic fever is carditis, or inflammation of the heart. This can affect all parts of the heart and can include pericarditis, myocarditis, endocarditis. Severe carditis can lead to symptoms consistent with acute heart failure such as fluid overload, shortness of breath, pulmonary hypertension, and death if untreated. Carditis is the most common cause of death in ARF patients.

Acute rheumatic fever is not always a once-occurring problem, and can happen to patients multiple times; patients with ARF are actually at high risk for recurrence of acute rheumatic fever exacerbations. As ARF is an autoimmune inflammatory disease, it makes sense that repeat streptococcus infections could cause the same autoimmune inflammatory problem repeatedly. Recurrent ARF is diagnosed when the Jones criteria is met; either two major criteria, one major and two minor criteria, or three minor criteria are fulfilled. This is slightly different from the initial exacerbation, which does not include diagnosis based only on three minor criteria.

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Acute Rheumatic Fever Treatment

Anti-inflammatories

Aspirin
NSAIDs
Glucocorticoids – not supported well by evidence

Symptomatic management

Heart failure treatment

Fluid management, positive pressure ventilation, surgery

Pain management
Psychosis

Chorea and psychosis can be prolonged
Average duration: 12-15 weeks

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As the primary causative factor in rheumatic fever exacerbations is inflammatory in nature, anti-inflammatories are the primary treatment option. Aspirin is inexpensive and is the most commonly used anti-inflammatory. Naproxen or ibuprofen are also acceptable anti-inflammatories commonly used.

Acute exacerbations of rheumatic fever are otherwise managed symptomatically. Of particular importance is management of heart failure symptoms, including diuresis to prevent fluid overload, positive pressure ventilation to reduce pulmonary edema, and surgical intervention if inflammation and scarring of the valves becomes extensive. Signs of left sided heart failure are more common in ARF patients because the left side of the heart is usually affected more by ARF than the right side. Signs of left sided heart failure include shortness of breath that is worse when laying flat, poor tolerance of reclining positions, coughing up pink frothy sputum, crackles on auscultation of lung sounds.

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Chronic Rheumatic Heart Disease

Long-term damage to heart
Staged as inactive, mild, moderate, or severe

Severe is most common at time of diagnosis
May improve or worsen over time

Mild	Moderate	Severe
Trivial to mild valve disease	Moderate valve lesion	Severe valve lesion
Heart murmur	Easily audible heart murmur	Loud heart murmur with thrill
Otherwise asymptomatic	Normal heart function	Signs of co-occurring heart failure
Not treated, monitored only	Usually monitored, seldom treated	Usually requires surgical repair

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Kawasaki Disease

Leading cause of acquired heart disease in the developed world
Abnormal autoimmune response to virus

Immune system attacks vasculature
Acute onset, self-limited

At least 4 out of 5 symptoms in addition to fever >5 days:

CRASH mnemonic

Can cause death if untreated

Usually requires ICU stay and extensive intervention

Anti-inflammatories, IVIG

High risk of coronary aneurysms

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Kawasaki disease is rare, but is the leading cause of acquired heart disease in the developed world. It is caused by an abnormal immune response to a virus. It is not certain which virus causes the reaction, but evidence points most strongly toward the Epstein-Barr virus, a common illness-causing virus.

The CRASH mnemonic stands for conjunctival irrigation, rash, adenopathy (cervical lymph), strawberry tongue, hands and feet erythematous with or without peeling. These symptoms must be present in the setting of a fever of at least 5 days that is not otherwise explained.

The primary cause of death is cardiac, as the vasculitis commonly leads to aneurisms, which can be an ongoing problem for patients even after they recover from an attack of Kawasaki’s. Treatment greatly reduces the risk of aneurisms, which improves survival rates dramatically. Though aspirin is normally contraindicated in febrile children due to the risk of Reyes syndrome, aspirin may be used as an anti-inflammatory in children with Kawasaki’s in an ICU setting. The gold standard treatment for Kawasaki’s is IVIG.

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What would the nurse do?

4 year old male patient
Evaluation for small size compared to peers
Immunized child, feeding difficulties during infancy, improved as child got older
Poor exercise tolerance, has difficulty running

and playing with other children

Lips frequently noted to be discolored
Notable exam findings:

Nail bed clubbing, trace cyanosis
Gr 2 heart murmur, lung sounds clear
Dyspnea noted with light exertion (walking to exam room)
Resting VS: P 120, R 36, BP 90/50

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Of particular concern in this case is the dyspnea with even light exertion and lip discoloration. These are all signs of poor oxygenation. We know this is a case of chronic poor oxygenation because of the nail bed clubbing; nail bed clubbing develops over years of hypoxemia and is not an acute finding. Poor exercise tolerance was noted by the caregiver, which tells us this problem has been occurring prior to their presentation today. His long history of poor feeding and small size compared to peers also point toward a heart problem.

This lecture is heart-oriented, so we know this is likely a heart problem case study. It is important to note that poor oxygenation has many potential causes, including heart problems, and that we need to narrow down causes if we want to help this child get the care they need. An issue that causes chronic hypoxia is likely to be either cardiac or respiratory in nature.

During today’s assessment, we noted a grade 2 heart murmur and some cyanosis in the nail beds. The heart murmur can point us toward a heart problem, but when assessing patients it is important to consider that murmurs are not always pathologic in nature, particularly grade 1 and 2 murmurs. Clear lung sounds is a pertinent negative finding, which means it is important to note even though the assessment finding is normal; this assessment finding helps guide our assessment away from a likely lung problem. The patient’s vital signs are somewhat abnormal; his resting heart rate is fast, but only 10 BPM above the normal finding for a child his age. His respiratory rate is also a little fast, but not severely so.

This child demonstrates many signs of a congenital heart defect and should be evaluated by a provider. The child will likely require further testing such as an echocardiogram and may require a surgical repair of the heart defect.

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What would the nurse do?

7 year old male
No previous known medical problems, immunized
6 day history of:

Fever 39C
Itchy eyes
Excessive fatigue, poor exercise tolerance

Physical exam findings

Gr 3 heart murmur, lung sounds clear
Bilateral conjunctivitis
Erythematous tongue

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A child presents with several normal signs of a benign illness; 3 days of fever, fatigue, and general malaise. He is noted to be otherwise healthy and immunized. This case, however, should throw up a few red flags that are worrisome findings. The new grade 3 heart murmur is the most obvious sign of a bigger problem. Conjunctivitis is very common in viral illnesses and is not necessarily worrisome by itself, but is one of the signs of more serious illness and is the third sign of Kawasaki disease, an inflammatory vasculitis usually caused by an abnormal immune response to a viral illness. The erythematous tongue (“strawberry tongue”) is another sign of Kawasaki’s.

This child will require immediate hospitalization and intervention to minimize damage to the heart and vascular structures. The nurse should notify the provider of these findings if they are not already aware, ensure vascular access is obtained (IV or IO), and anticipate drawing blood for laboratory studies.

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What would the nurse do?

5 year old female
No previous known medical problems, immunized
Complaint of chest pain started yesterday
Illness with sore throat, rash 2-3 weeks ago, resolved
Physical exam:

Gr 2 heart murmur
Uncontrolled movements of all 4 extremities
Anxiety, agitation during exam
Fever 38.5C

Contact info: info@nursesinternational.org

This child is presenting with 2 of the major Jones criteria for acute rheuamtic fever (carditis, exemplified by chest pain that is new, and the uncontrolled movements of the extremities), which is adequate for diagnosis of acute rheumatic fever.

The nurse should notify the provider of the symptoms and concerns for acute rheumatic fever. The nurse should anticipate blood testing including inflammatory markers like CRP, ESR, and insertion of an IV in case heart failure management needs to take place. The child will also need an EKG and will likely be given anti-inflammatories like aspirin.

Teaching points for the parents should include preparation for a likely hospital stay, management with anti-inflammatory medications, risks of developing chronic rheumatic heart disease, and warning signs for recurrence of acute rheumatic fever.

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Glossary

Ductus Arteriosus- a fetal blood vessel that connects the left pulmonary artery directly to the descending aorta, normally closing after birth
portal sinus-a vein carrying blood from the digestive organs and spleen to the liver
foramen ovule- an opening in the septum between the two atria of the heart that is normally present only in the fetus
syncope- loss of consciousness resulting from insufficient blood flow to the brain
hypoxia- a deficiency of oxygen reaching the tissues of the body
dyspnea-difficult or labored respiration
cyanotic- a bluish or purplish discoloration (as of skin) due to deficient oxygenation of the blood
rheumatic-any of various conditions characterized by inflammation or pain in muscles, joints, or fibrous tissue

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References

Cannon, J., Roberts, K., Milne, C., & Carapetis, J. (2017). Rheumatic heart disease severity, progression, and outcomes: A multi-state model. Journal of the American Heart Association, 6(3).

Essop, M., & Peters, F. (2014). Contemporary issues in rheumatic fever and chronic rheumatic heart disease. Circulation, 130(24), 81-88. Frank, J., Jacobe, K. (2011). Evaluation and management of heart murmurs in children. American Family Physician, 84(7), 793-800.

Friedman, A., & Fahey, J. (1993). The transition from fetal to neonatal circulation: Normal responses and implications for infants with heart disease. Seminars in Perinatology, 17(2), 106-121.

Jarvis, C. (2015). Physical examination & health assessment (7th ed.). Philadelphia, PA: Elsevier Health Sciences.

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