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Carditis, or inflammation of the heart, is most conveniently broken down into three categories:

  • Pericarditis - Inflammation of the pericardium
    • The pericardium is a double-walled fibroserous sac that surrounds and supports the heart. Normally, 15 to 50 ml of fluid separates the two layers. In pericarditis, the pericardium becomes inflamed. Excess fluid may accumulate in this space, resulting in a pericardial effusion.
  • Myocarditis - Inflammation of the heart muscle
  • Endocardistis - Inflammation of the endocardium
    • The endocardium is the innermost layer of the heart and includes the valves, chordae tendineae, cardiac septum, or the lining of the chambers.

PERICARDITIS

  • Pericarditis, inflammation of the fibroserous sac enclosing the heart, manifests itself as one of three types as a result of the bodies reaction to the infecting agent:
    • Acute serofibrinous pericarditis - the result of virus infection
    • Acute purulent pericarditis - the result of bacterial infection (except for infection by Mycobacterium tuberculosis)
    • Chronic pericarditis - the result of infection by M. tuberculosis or fungi
  • Etiology:
    • Virtually any infectious agent that reaches the pericardium is capable of causing pericarditis. The most common viruses causing the disease are members of the Picornaviridae (enteroviruses) while the most common bacteria infecting the pericardium are the pyogenic cocci (Staphylococcus, Streptococcus, Neisseria). Chronic pericarditis is most commonly caused by M. tuberculosis or Histoplasma capsulatum.
  • Clinical Symptoms & Signs:
    • Acute sero-fibrinous pericarditis gives rise to:
      • a. Chest pain - rapid in onset, persistent for several hours to days. It is worse during inspiration and recumbency but improves with leaning forward. The pain is usually in the upper abdominal region overlying the stomach and may be sharp, dull, constricting and/or crushing making clinical differentiation from myocardial infarction difficult. Radiation of pain to the left trapezius ridge is particularly characteristic.
      • b. Fever - not prominent
      • c. Malaise
      • d. Pericardial friction rub - this is usually a triphasic sound that resembles scratching or the crunch of footsteps on cold snow.
    • Acute purulent pericarditis gives rise to:
      • a. Little, if any, chest pain
      • b. Prominent fever and chills from the severe underlying infection
      • c. Cardiac tamponade which leads to: (1) Dyspnea; (2) Agitation; (3) Orthopnea; (4) Cough
      • d. Pericardial friction rub - occurs in less than 50% of patients.
    • Chronic pericarditis is generally due to M. tuberculosis and the symptoms are those of tuberculosis. These include:
      • a. Fever
      • b. Night sweats
      • c. Weight loss
      • d. Fatigue
      • e. Progressive circulatory failure due to: (1) Slowly progressing dyspnea; (2) Ascites; (3) Edema

  • In general, all types of pericarditis may result in:
    • a. Abnormal heart sounds other than those due to pericardial friction
    • b. Pericardial effusion that causes:
      • (1) Decreased or muffled heart sounds
      • (2) An area of dullness to percussion at the tip of the left scapula (Ewart's sign)
      • (3) Pulsus paradoxes
      • (4) Cervical venous pressure increase with inspiration (Kussmaul's sign)
      • (5) Abnormal EKG

Myocarditis

  • The disease is an infection of the myocardium or muscle of the heart. The virus is ingested in fecal-contaminated water and/or food and eventually, either directly or indirectly, reaches the heart. There may be a prior skin infection before heart effects are seen. The virus invades the heart muscle cells and causes necrosis of the cells and clinical effects.
  • Many species of viruses, bacteria, chlamydia, rickettsia, fungi and protozoans can cause myocarditis. However, viruses are the most important infectious agents. Of these, the enteroviruses are the single most important group.
  • If not treated, it can lead to coronary artery thrombus, coronary ischemia, dilated cardiomyopathy, cardiac arrhythmias, and sudden death.
  • Although usually mild, this inflammation of the heart muscle can be fatal.
  • Diagnosis:
    • In infants and young children, the disease progresses rapidly, beginning with fever, tachycardia and listlessness and progressing with signs and symptoms of CNS, gastrointestinal, liver and myocardial involvement. Cardiac failure may be evident within a few days of onset of the illness.
    • In older children and adults, the illness usually progresses more slowly with generalized manifestations of viral infections localized to:
      • a. Respiratory tract
        • (1) Moderate fever
        • (2) Cough
        • (3) Coryza
      • b. Abdomen
        • (1) Pain
        • (2) Nausea
        • (3) Vomiting
  • Myocardial involvement becomes manifest one or two weeks after the initial illness with:
    • a. Fever
    • b. Malaise
    • c. Fatigue
    • d. Dyspnea (labored or difficult breathing)
    • e. Palpitations (tachycardia)
    • f. Altered heart sounds (muffled, transient pericardial rubs)
    • g. Chest pain
    • h. Electrocardiographic changes
    • i. Cardiomegaly
    • j. Pulmonary congestion
    • k. Abnormal laboratory findings: (1) Increased sedimentation rate; (2) Increased leukocyte count; (3) Increased myocardial isoenzymes

ENDOCARDITIS

  • Endocarditis, inflammation of the membrane lining the chambers of the heart and covering the cusps of the various valves, is caused directly by microbial colonization of the endocardium or indirectly by induction of autoimmunity, as in acute rheumatic fever. Direct colonization is termed infective endocarditis and is caused by microorganisms physically present in endocardial lesions know as vegetations. The disease may be either acute or chronic.
  • Almost all bacteria and many fungi, when they get into the blood stream, can cause infective endocarditis. However, 80% of the cases are caused by streptococci or staphylococci.
  • Clinical Symptoms:
    • The interval between the colonization of the endocardium and the onset of symptoms is two weeks.
    • Heart murmur is present at some times during the disease but is generally not constant. If the tricuspid valve is damaged to the extent that there is tricuspid regurgitation, Carvallo's sign will be present; this is augmentation of the pan-cystolic murmur by inspiration.
    • Death can occur about 6 weeks after colonization if the disease goes untreated.
    • The initial symptoms are those of any infection:
      • a. Low grade fever
      • b. Anorexia
      • c. Fatigue
      • d. Weight loss
      • e. Anemia
      • f. Splenomegaly
    • The circulating immune complexes give rise to skin manifestations which include:
      • a. Osler's nodes
      • b. Splinter hemorrhages
      • c. Petechia
      • d. Janeway's lesions
      • e. Roth spots
    • Urinary findings may include:
      • a. Proteinuria
      • b. Microscopic hematuria
      • c. Red blood cell casts
  • Diagnosis:
    • Because the clinical features of the disease can be quite variable and often nonspecific, diagnosis is mainly based on laboratory tests. Blood culture and serologic testing are the most important. Always use venous blood to isolate the organism. A positive blood culture with some or all of the symptoms listed is needed to obtain the diagnosis.

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