UNIVERSITY OF EASTERN AFRICA, BARATON

SCHOOL OF NURSING

DEPARTMENT OF MATERNAL AND CHILD HEALTH NURSING

A PRESENTATION DONE IN PARTIAL FULFILLMENT OF THE

COURSE: CHILD HEALTH NURSING.

COURSE CODE: NRSG 328. PEDIATRIC NURSING

TOPIC: MYOCARDITIS

NAME: AMOS KIPROTICH MELI SAMOME2111

MERCY CHEROTICH SMERCH2022

INSTRUCTOR: MADAM MARY MYAGISERA

DUE DATE: 15TH ,MAY2023.

MYOCARDITIS.
Introduction.
Myocarditis is a condition where the muscular walls of the heart become inflamed. Can be
acute or chronic. It is characterized by inflammatory cell infiltrates, myocyte necrosis or
myocyte degeneration.

Causes
a) Viral infection coxsackie viruses, Influenza virus, Cytomegalovirus, poxvirus,
Parvovirus, Rubella, Varicella and Epstein Barr virus.
b) Bacterial infections. Meningococcus, Klebsiella spp, Staphylococcus and Treponema
pallidum.
c) Autoimmune disorders such as SLE
d) Other causes
Protozoa e.g., trypanosoma cruzi, amoeba.
Yeast e.g., candida.
Toxin e.g., diphtheria, scorpion.
Drugs e.g., sulfonamides.
Risk factors
Immunosuppression due to organ transplant
Age
Gender
Genetic predisposition
Recent viral illness or vaccination especially those targeting respiratory viruses
Carbon monoxide poisoning
Pathophysiology.
The etiological factors above, the most common cause in children is coxsackie viruses which
on exposure to child triggers inflammation of the myocardium the middle layer of heart
muscles this inflammation triggers immune response which release various immune cells and
chemicals mediators to fight the infection. The immune system is regulated by CD4 T-helper
cells and CD8 cytotoxic T cells which are stimulated along with proinflammatory Cytokines.
In some cases, the response is dysregulated resulting in excess inflammatory reaction. The
immune cells may infiltrate into the cardiac tissue and myocytes resulting in further
inflammation and myocyte injury and dysfunction. There is also release of intracellular
component into the bloodstream such as protein troponin produced by damaged myocytes.
This infiltrated immune cells further release reactive oxygen species such as nitric oxide
which has been been linked to myocardial tissue damage. Inflammation and the myocyte
damage leads to decreased myocardial contractility; heart enlarges leading to decreased
cardiac output.
Clinical manifestation.
Myocarditis symptoms and signs appears flu like and range from asymptomatic to
nonspecific generalized illness to acute cardiogenic shock and sudden death.Infants often
have a sudden presentation characterized with-
Fever caused by detection of pathogen triggers inflammatory process with release of
pyrogens
Respiratory distress. Decreased cardiac output means inadequate oxygenation and pulmonary
congestion.
Tachycardia. -inflammatory process results in conduction abnormalities which lead to rapid
and irregular heart rate
Cardiogenic shock-occurs when the heart is unable to pump enough blood to meet the body
need and hypotension manifest as low blood pressure and pale extremities
Edema due to fluid retention and impaired circulation which cause fluid to accumulate in
tissues
Fatigue and weakness-due to decreased cardiac output to resulting in inadequate perfusion in
various organs
Chest pain and tightness which worsen on physical activities
Gallop rhythm and Cardiac murmur effect of myocarditis on heart electrical system leading to
abnormal heart rhythms
DIAGNOSIS:
a) Electrocardiographic Changes:
Sinus tachycardia: Faster-than-normal heart rate.
Atrial and ventricular arrhythmias: Irregular heart rhythms originating from the atria or
ventricles.
Heart block: Impaired electrical signals between the atria and ventricles.
Diminished QRS voltages: Reduced amplitudes of the QRS complex on the
electrocardiogram (ECG).
Nonspecific ST and T wave changes suggesting acute ischemia: Abnormalities in the ST
segment and T wave on the ECG, indicating potential inadequate blood supply to the heart.
b) Chest X-ray:
Cardiomegaly: Enlargement of the heart.
Pulmonary vascular prominence: Increased visibility and prominence of blood vessels in the
lungs.
Overt pulmonary edema or pleural effusions: Accumulation of fluid in the lungs or the space
around the lungs.
c) Cardiac MRI:
Presence of edema: Swelling or fluid accumulation within the heart muscle.
Myocyte necrosis: Cell death or damage in the heart muscle cells.
Left ventricular dysfunction: Impaired function of the heart's left ventricle, responsible for
pumping oxygenated blood to the body.
d) Endomyocardial Biopsy:
Identify inflammatory cell infiltrates or myocyte damage: Examining tissue samples taken
from the heart to identify the presence of immune cells or damage to heart muscle cells.
Perform molecular viral analysis using polymerase chain reaction techniques: Using
laboratory methods to detect viral genetic material in the heart tissue.
e) Nonspecific Tests:
Sedimentation rate: A blood test that measures the rate at which red blood cells settle in a test
tube, indicating the presence of inflammation.
Creatinine phosphokinase (CPK) enzymes: Blood tests that assess the levels of CPK
enzymes, which may indicate muscle damage.
MEDICAL MANAGEMENT:
Supportive Care: This includes measures to manage symptoms and maintain organ function.
Patients may require hospitalization and bed rest. Oxygen therapy, intravenous fluids, and
electrolyte replacement may be necessary. Cardiac monitoring is essential, including
continuous electrocardiogram (ECG) monitoring and echocardiography.
Anti-inflammatory medications: non-steroidal anti-inflammatory drugs (NSAIDs), such as
ibuprofen and naproxen, and corticosteroids like prednisone and methylprednisolone can be
used to reduce inflammation and relieve symptoms. However, caution should be taken as the
evidence for the efficacy of these medications in treating myocarditis is limited.
Nonsteroidal anti-inflammatory drugs (NSAIDs):
Ibuprofen: 10 mg/kg/dose every 6-8 hours (up to 40 mg/kg/day)
Naproxen: 5-10 mg/kg/dose every 12 hours (up to 20 mg/kg/day)
Corticosteroids:
Prednisone: 1-2 mg/kg/day divided into 2-3 doses
Methylprednisolone: 1-2 mg/kg/day divided into 2-3 doses
Immunosuppressive therapy: If the underlying cause of the myocarditis is an autoimmune
disorder, immunosuppressive drugs like azathioprine and cyclosporine may be prescribed to
suppress the immune system.
Azathioprine: 1-2 mg/kg/day
Cyclosporine: 5-10 mg/kg/day divided into 2 doses
Diuretics
May be prescribed to manage fluid overload or congestion occurring as a result of
myocarditis induced heart failure
Furosemide: neonates 1-4mg/kg 1-2 times/day
Children > 1month 2mg/kg maximum dose of 6mg/kg
Inotropic
In severe cases with significant cardiac dysfunction, they may be used to improve cardiac
contractility and support the heart’s pumping function
Dobutamine: 2-15mcg/kg/min
Milrinone: loading dose 50mcg/kg over 10mins followed by continuous infusion at
0.5mcg/kg/min
Treatment for underlying infections: Antibiotics, antiviral drugs, or other medications may
be necessary if an infection is identified as the underlying cause of myocarditis.
Mechanical circulatory support: In severe cases where the heart is unable to pump
effectively, mechanical circulatory support such as extracorporeal membrane oxygenation
(ECMO) may be required.
NURSING MANAGEMENT:
- Heart rate, respiratory rate and blood pressure should be monitored frequently.
- Fluid intake and urine output monitoring is mandatory.
- All patients require bed rest.

NURSING DIAGNOSIS
Decreased Cardiac Output related to impaired myocardial contractility as evidenced by
decreased peripheral perfusion, diminished heart sounds, and altered cardiac rhythm.
Risk for Decreased Tissue Perfusion related to compromised cardiac function
Activity Intolerance related to decreased cardiac function as evidenced by fatigue, dyspnea,
and decreased exercise tolerance.
REFERENCE:
o Hockenberry.M. Wongs Essentials of Pediatric Nursing 8th Ed. Mosby 2009
o A manual for pediatric house officer The Harriet lane handbook,the John's Hopkins hospital
22nd edition. Philadelphia