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MS.B.SHYLA MERCY
M. SC (N) , MEDICAL SURGICAL NURSING
LECTURER
GANGA COLLEGE OF NURSING
COIMBATORE
MYOCARDITIS
INTRODUCTION
• Myocarditis is an inflammatory disease of the myocardium caused by
different infectious and noninfectious triggers .
• In 1995, myocarditis was defined by the World Health Organization
(WHO)/International Society and Federation of Cardiology (ISFC) as an
inflammatory disease of the heart muscle, diagnosed by established
histological, immunological, and immunohistochemical criteria
• Cases of Myocarditis have been documented as early as the 1600s, but the
term "Myocarditis", implying an inflammatory process of the
myocardium, was introduced by German physician Joseph Friedrich
Sobernheim in 1837.
HISTORICALASPECTS
❖1837 - J.F.Soberenheim first used the term “ Myocarditis”.
❖1897 - M.O.Abramov described pathological changes in myocarditis.
❖1990 - F.Fidler described primary idiopathic myocarditis.
❖1920s - There was overdiagnosis of myocarditis.
❖1920-50s - The term myocarditis replaced the term “Degeneration of the myocardium”
❖1949 - I. Gore ., O.Sapfir described viral and rikettsial myocarditis.
❖1980s - There was an introduction of transvenous myocardial biopsy into clinical
practice.
❖ 1992 - M .Paleev define the term “myocarditis” is a heart muscle lesion mainly of
inflammatory nature caused by influence of infection, parasitic , physical agents
or when develop in autoimmune diseases.
DEFINITION
Myocarditis is defined as the
inflammation of myocardium, can cause
heart dilation, thrombi on the heart wall
and infiltration of circulatory blood cells
around the coronary vessels and resulted
in degeneration of muscle fibres.
EPIDEMIOLOGY
1-9 % of all patients had
evidence of myocardial
inflammation.
In young adults , up to 20% of
all cases of sudden death are
due to myocarditis.
The incidence of myocarditis is
approximately 1.5 million cases
worldwide per year.
TYPES OF MYOCARDITIS
• ACUTE MYOCARDITIS
• SUBACUTE MYOCARDITIS
• CHRONIC MYOCARDITIS
1) ACUTE MYOCARDITIS
• Acute myocarditis is commonly
caused by a viral infection that
produces myocardial necrosis
and triggers an immune
response to eliminate the
infectious agent .
STAGES OF VIRAL MYOCARDIUM INFECTION
2) SUBACUTE
MYOCARDITIS
• Subacute phase, which covers few
weeks to several months, is defined
by activated virus-specific
T lymphocytes, which may target the
host’s organs by molecular mimicry.
• Cytokine activation (tumor necrosis
factor alpha, interleukin [IL] and
antibodies to viral and cardiac
proteins may aggravate cardiac
damage and cause impairment of the
contractile function.
3) CHRONIC MYOCARDITIS
• Structural and functional damage of the myocardium,
activates the innate and adaptive immune response, which
can lead to severe inflammation .
• The immune response is eventually downregulated, and
myocardial inflammation can also persist.
• Persistent inflammation is characterized by an ongoing
damage to the cardiomyocytes and ultimately results in
dilated cardiomyopathy (DCM)
ETIOLOGICAL FACTORS OF
MYOCARDITIS
1.Infectious
2.Non-Infectious
INFECTIOUS
MYOCARDITIS
1-Viral: Coxsackievirus B, parvovirus B19 (common),Human
Herpes virus 6, HFVs and others.
2-Bacterial: Treponema palladium (Syphilis) and Borrelia
burgdorferi (Lyme disease) and Rickettsia.
3-Protozoal: Chagas disease (common), Toxoplasmosis.
4-Helminthes: Trichinella spiralis, Ascaris, Echinococcus
granulosus, Schistosoma, Taenia solium, and Wuchereria
bancrofti.
5-Fungal: Blastomycosis, Coccidiomycosis,Cryptococcosis,
and Aspergillosis.
NON-INFECTIOUS MYOCARDITIS
1)Autoimmune reaction due to infection or systemic
disorder:
• A-Exogenous Antigen:
• Post-Streptococcus pyogenes autoimmune reaction.(Acute
rheumatic fever).
• B-Endogenous Antigen:
• systemic lupus erythematosus , and systemic vasculitis.
• 2)Cardiotoxins(Drug-induced Myocarditis):
• A-Toxins associated with hypersensitivity reaction:
• Toxic shock syndrome toxin, Snake venom, antibiotics.
• B-Toxic Myocarditis: Carbon monoxide, Heavy metals&
Ethanol.
PATHOPHYSIOLOGY
CLINICAL
MANIFESTATIONS
EARLY SYSTEMIC MANIFESTATION
Fatigue
Malaise
Myalgia
Pharyngitis
Dyspnea
Lymphadenopathy
Nausea and vomiting.
Fever
EARLY CARDIAC SIGNS
➢Pleuritic chest pain
➢Pericardial friction rub
➢Pericardial effusion
LATE CARDIAC SIGNS
➢S3 heart sound
➢Crackles
➢Syncope
➢Angina
PLEURITIC CHEST PAINPERICARDIAL FRICTION RUB
PERIPHERAL EDEMA JUGULAR VEIN DISTENTION
DIAGNOSTIC EVALAUTION
1. HISTORY COLLECTION
History of Rheumatic fever .
2. PHYSICAL EXAMINATION
• Peripheral Edema
• Auscultation of Heart and Lung Sounds
• Jugular vein distension.
3. BLOOD TESTS
• Leukocytosis
• Elevated ESR and CRP level
• Elevated levels of Myocardial markers such as troponin
• Elevated Viral titers
4) ELECTROCARDIOGRAM
Diffuse ST Segment Changes
5) ENDOMYOCARDIAL BIOPSY
• Histologic confirmation of myocarditis is
through an Endomyocardial biopsy.
• A biopsy done during the first 6 weeks of
acute illness .
6) NUCLEAR SCANS
7) ECHOCARDIOGRAPHY
8) MRI
MANAGEMENT
• PHARMACOLOGICAL MANAGEMENT
• SUPPORTIVE THERAPY
• DIETARY&LIFESTYLE
• NURSING MANAGEMENT
Myocarditis resolves in about 50% of cases in the first 2–4
weeks, but about 25% will develop persistent cardiac
dysfunction and
12–25% may acutely deteriorate and either die or progress to
end-stage DCM with a need for heart transplantation.
The core principles of treatment in myocarditis are
optimal care of Arrhythmia and Heart failure
PHARMACOLOGICAL MANAGEMENT
1) ANGIOTENSIN - CONVERTING ENZYME INHIBITORS
Captopril , Lisinopril and Ramipril relax the blood vessels in heart and
help blood flow more easily.
2) ꞵ - ADRENERGIC BLOCKERS
Metoprolol ,Bisoprolol and Carvedilol to treat heart failure and control
arrhythmias.
3) DIURETICS
Furosemide to relieve sodium and fluid retention.
4) IMMUNOSUPPRESSIVE THERAPY
5) ANTICOAGULATION THERAPY
DIGOXIN
It improves myocardial contractility and reduces the heart rate.
It is used cautiously in a patients with myocarditis , since the
condition predisposes patients to drug related dysrhythmias and
toxicity.
TREATMENT GUIDELINES
SUPPORTIVE
THERAPY
• Oxygen therapy
• Bed rest
• Restricted activity
IN CASES OF SEVERE HEART FAILURE
INTRAAORTIC BALLOON
THERAPY VENTRICULAR ASSIST DEVICES
DIETARY& LIFESTYLE MANAGEMENT
1) Restrict salt intake to 2-3 gm of sodium per
day.
2) Restrict the amount of fluids you drink and
avoid smoking.
3) Rest and reducing the workload on your heart .
4) Exercise especially during the acute phase of
virus myocarditis enhances viral replication
rate, enhances immune mechanisms and
increases inflammatory lesions and necrosis.
5) Resumption of physical activity can take place
within 2 months of the acute disease.
• Assess complaints of chest pain, observe the factors that
aggravate. Notice the nonverbal cues of discomfort.
• Assess vital signs and cardiovascular assessment.
• Evaluate patients' pulse and apical rate for signs of
tachycardia and gallop rhythm indications that heart failure
is recurring.
• Ensure measures to decrease cardiac workload.
• Passive and active exercises , Elastic compression stockings to
prevent venous thrombosis.
NURSING MANAGEMENT
NURSING DIAGNOSIS
❖Acute chest pain related to
myocardial inflammation as
evidenced by pain score.
❖Decreased cardiac output related
to degeneration of heart muscle
as evidenced by tachycardia.
❖Impaired peripheral tissue
perfusion related to reduced
cardiac output.
COMPLICATIONS
CONCLUSION
Myocarditis is an inflammatory disease of the heart frequently
resulting from viral infections or post-viral immune-mediated
responses. It is one of the important causes of dilated
cardiomyopathy worldwide.
Endomyocardial biopsy remains the gold standard for in vivo
diagnosis of myocarditis. Treatment for myocarditis consists
of managing associated heart symptoms.
BIBLIOGRAPHY
➢Bare,G.Brenda, Smelter and Suzanne (2014).Brunner and suddarth’s “Text Book of
Medical Surgical Nursing”10th edition .Philadelphia .Lippincott publications.
➢Meg Gulanick (2018). “Nursing Care Plan, Diagnoses, Interventions and Outcomes”
9th edition .St. Louis united states .Elsevier publications.
➢April hazard ,Judith (2018), “ Davis's Drug Guide for Nurses” 16th edition
Philadelphia .F.A. Davis company publication.
MYOCARDITIS
MYOCARDITIS

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MYOCARDITIS

  • 1. MS.B.SHYLA MERCY M. SC (N) , MEDICAL SURGICAL NURSING LECTURER GANGA COLLEGE OF NURSING COIMBATORE
  • 3.
  • 4.
  • 5. INTRODUCTION • Myocarditis is an inflammatory disease of the myocardium caused by different infectious and noninfectious triggers . • In 1995, myocarditis was defined by the World Health Organization (WHO)/International Society and Federation of Cardiology (ISFC) as an inflammatory disease of the heart muscle, diagnosed by established histological, immunological, and immunohistochemical criteria • Cases of Myocarditis have been documented as early as the 1600s, but the term "Myocarditis", implying an inflammatory process of the myocardium, was introduced by German physician Joseph Friedrich Sobernheim in 1837.
  • 6. HISTORICALASPECTS ❖1837 - J.F.Soberenheim first used the term “ Myocarditis”. ❖1897 - M.O.Abramov described pathological changes in myocarditis. ❖1990 - F.Fidler described primary idiopathic myocarditis. ❖1920s - There was overdiagnosis of myocarditis. ❖1920-50s - The term myocarditis replaced the term “Degeneration of the myocardium” ❖1949 - I. Gore ., O.Sapfir described viral and rikettsial myocarditis. ❖1980s - There was an introduction of transvenous myocardial biopsy into clinical practice. ❖ 1992 - M .Paleev define the term “myocarditis” is a heart muscle lesion mainly of inflammatory nature caused by influence of infection, parasitic , physical agents or when develop in autoimmune diseases.
  • 7. DEFINITION Myocarditis is defined as the inflammation of myocardium, can cause heart dilation, thrombi on the heart wall and infiltration of circulatory blood cells around the coronary vessels and resulted in degeneration of muscle fibres.
  • 8.
  • 9. EPIDEMIOLOGY 1-9 % of all patients had evidence of myocardial inflammation. In young adults , up to 20% of all cases of sudden death are due to myocarditis. The incidence of myocarditis is approximately 1.5 million cases worldwide per year.
  • 10. TYPES OF MYOCARDITIS • ACUTE MYOCARDITIS • SUBACUTE MYOCARDITIS • CHRONIC MYOCARDITIS
  • 11. 1) ACUTE MYOCARDITIS • Acute myocarditis is commonly caused by a viral infection that produces myocardial necrosis and triggers an immune response to eliminate the infectious agent .
  • 12. STAGES OF VIRAL MYOCARDIUM INFECTION
  • 13. 2) SUBACUTE MYOCARDITIS • Subacute phase, which covers few weeks to several months, is defined by activated virus-specific T lymphocytes, which may target the host’s organs by molecular mimicry. • Cytokine activation (tumor necrosis factor alpha, interleukin [IL] and antibodies to viral and cardiac proteins may aggravate cardiac damage and cause impairment of the contractile function.
  • 14. 3) CHRONIC MYOCARDITIS • Structural and functional damage of the myocardium, activates the innate and adaptive immune response, which can lead to severe inflammation . • The immune response is eventually downregulated, and myocardial inflammation can also persist. • Persistent inflammation is characterized by an ongoing damage to the cardiomyocytes and ultimately results in dilated cardiomyopathy (DCM)
  • 16. INFECTIOUS MYOCARDITIS 1-Viral: Coxsackievirus B, parvovirus B19 (common),Human Herpes virus 6, HFVs and others. 2-Bacterial: Treponema palladium (Syphilis) and Borrelia burgdorferi (Lyme disease) and Rickettsia. 3-Protozoal: Chagas disease (common), Toxoplasmosis. 4-Helminthes: Trichinella spiralis, Ascaris, Echinococcus granulosus, Schistosoma, Taenia solium, and Wuchereria bancrofti. 5-Fungal: Blastomycosis, Coccidiomycosis,Cryptococcosis, and Aspergillosis.
  • 17. NON-INFECTIOUS MYOCARDITIS 1)Autoimmune reaction due to infection or systemic disorder: • A-Exogenous Antigen: • Post-Streptococcus pyogenes autoimmune reaction.(Acute rheumatic fever). • B-Endogenous Antigen: • systemic lupus erythematosus , and systemic vasculitis. • 2)Cardiotoxins(Drug-induced Myocarditis): • A-Toxins associated with hypersensitivity reaction: • Toxic shock syndrome toxin, Snake venom, antibiotics. • B-Toxic Myocarditis: Carbon monoxide, Heavy metals& Ethanol.
  • 20. EARLY CARDIAC SIGNS ➢Pleuritic chest pain ➢Pericardial friction rub ➢Pericardial effusion LATE CARDIAC SIGNS ➢S3 heart sound ➢Crackles ➢Syncope ➢Angina
  • 22. PERIPHERAL EDEMA JUGULAR VEIN DISTENTION
  • 23. DIAGNOSTIC EVALAUTION 1. HISTORY COLLECTION History of Rheumatic fever . 2. PHYSICAL EXAMINATION • Peripheral Edema • Auscultation of Heart and Lung Sounds • Jugular vein distension. 3. BLOOD TESTS • Leukocytosis • Elevated ESR and CRP level • Elevated levels of Myocardial markers such as troponin • Elevated Viral titers
  • 25. 5) ENDOMYOCARDIAL BIOPSY • Histologic confirmation of myocarditis is through an Endomyocardial biopsy. • A biopsy done during the first 6 weeks of acute illness . 6) NUCLEAR SCANS 7) ECHOCARDIOGRAPHY
  • 27. MANAGEMENT • PHARMACOLOGICAL MANAGEMENT • SUPPORTIVE THERAPY • DIETARY&LIFESTYLE • NURSING MANAGEMENT
  • 28. Myocarditis resolves in about 50% of cases in the first 2–4 weeks, but about 25% will develop persistent cardiac dysfunction and 12–25% may acutely deteriorate and either die or progress to end-stage DCM with a need for heart transplantation. The core principles of treatment in myocarditis are optimal care of Arrhythmia and Heart failure
  • 29. PHARMACOLOGICAL MANAGEMENT 1) ANGIOTENSIN - CONVERTING ENZYME INHIBITORS Captopril , Lisinopril and Ramipril relax the blood vessels in heart and help blood flow more easily. 2) ꞵ - ADRENERGIC BLOCKERS Metoprolol ,Bisoprolol and Carvedilol to treat heart failure and control arrhythmias. 3) DIURETICS Furosemide to relieve sodium and fluid retention. 4) IMMUNOSUPPRESSIVE THERAPY 5) ANTICOAGULATION THERAPY
  • 30. DIGOXIN It improves myocardial contractility and reduces the heart rate. It is used cautiously in a patients with myocarditis , since the condition predisposes patients to drug related dysrhythmias and toxicity.
  • 32. SUPPORTIVE THERAPY • Oxygen therapy • Bed rest • Restricted activity
  • 33. IN CASES OF SEVERE HEART FAILURE INTRAAORTIC BALLOON THERAPY VENTRICULAR ASSIST DEVICES
  • 34. DIETARY& LIFESTYLE MANAGEMENT 1) Restrict salt intake to 2-3 gm of sodium per day. 2) Restrict the amount of fluids you drink and avoid smoking. 3) Rest and reducing the workload on your heart . 4) Exercise especially during the acute phase of virus myocarditis enhances viral replication rate, enhances immune mechanisms and increases inflammatory lesions and necrosis. 5) Resumption of physical activity can take place within 2 months of the acute disease.
  • 35. • Assess complaints of chest pain, observe the factors that aggravate. Notice the nonverbal cues of discomfort. • Assess vital signs and cardiovascular assessment. • Evaluate patients' pulse and apical rate for signs of tachycardia and gallop rhythm indications that heart failure is recurring. • Ensure measures to decrease cardiac workload. • Passive and active exercises , Elastic compression stockings to prevent venous thrombosis. NURSING MANAGEMENT
  • 36. NURSING DIAGNOSIS ❖Acute chest pain related to myocardial inflammation as evidenced by pain score. ❖Decreased cardiac output related to degeneration of heart muscle as evidenced by tachycardia. ❖Impaired peripheral tissue perfusion related to reduced cardiac output.
  • 38. CONCLUSION Myocarditis is an inflammatory disease of the heart frequently resulting from viral infections or post-viral immune-mediated responses. It is one of the important causes of dilated cardiomyopathy worldwide. Endomyocardial biopsy remains the gold standard for in vivo diagnosis of myocarditis. Treatment for myocarditis consists of managing associated heart symptoms.
  • 39. BIBLIOGRAPHY ➢Bare,G.Brenda, Smelter and Suzanne (2014).Brunner and suddarth’s “Text Book of Medical Surgical Nursing”10th edition .Philadelphia .Lippincott publications. ➢Meg Gulanick (2018). “Nursing Care Plan, Diagnoses, Interventions and Outcomes” 9th edition .St. Louis united states .Elsevier publications. ➢April hazard ,Judith (2018), “ Davis's Drug Guide for Nurses” 16th edition Philadelphia .F.A. Davis company publication.