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Inflammatory Disorders. TISSUES SURROUNDING THE HEART. Layers of the Heart Muscle. Etiology/Pathophysiology. Endocarditis When valve damaged, blood is slowed down and forms a clot. Bacteria get into blood stream

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Presentation Transcript
etiology pathophysiology
  • Endocarditis
    • When valve damaged, blood is slowed down and forms a clot.
    • Bacteria get into blood stream
    • Bacterial or fungal vegetative growths deposit on normal or abnormal heart valves
classifications of endocarditis
Classifications of Endocarditis
  • Acute Infective Endocarditis
    • Abrupt onset
    • Rapid course
    • Staph Aureus
  • Subacute Infective Endocarditis SBE
    • Gradual onset
    • Systemic manifestations
  • Prosthetic Valve Endocarditis
    • Occurs within 2 months after OR
risk factors endocarditis
Risk Factors- endocarditis
  • Hx of rheumatic fever or damaged heart valve
  • Invasive procedures- dental,gyne, etc.
  • IV drug users
  • Valve replacements
assesment endocarditis
Assesment endocarditis
  • Infection and emboli
    • Emboli-spleen most often affected
    • Osler’s nodes
    • Splinter hemorrhages
    • Janeway lesions
    • Murmur
    • T above 101(blood cultures),chills
    • Anorexia
    • Fatigue
    • Roth spots

Osler’s nodes

Janeway lesions

Splinter hemmorrhages

Roth spots

diagnostic tests
Diagnostic Tests
  • Blood Cultures- for temp >101
  • Echocardiogram-TEE best- see vegetations
  • Other- CBC,ESR, serum creatinine,CXR, and EKG
  • Antibiotics
    • IV for 2-8 weeks
    • Monitor peaks and troughs of certain drugs
    • Monitor BUN and Creat.
nursing diagnoses
Nursing Diagnoses
  • Risk for Imbalanced Body Temperature
  • Risk for Ineffective Tissue Perfusion-emboli
  • Ineffective Health Maintenance
  • Emboli(50% incidence)
    • Right side- pulmonary emboli
    • Left side-brain, spleen, heart, limbs,etc
  • CHF-check edema, rales, VS
  • Arrhythmias-Afib most common
  • Death
  • Cardiac Tamponade


  • Eliminate risk factors
  • Patient teaching
    • Penicillin prophylaxis
etiology pathophysiology1
  • Myocarditis
    • Virus, toxin or autoimmune response causes necrosis of the myocardium
    • Frequently caused by Coxsackie B virus
    • Get dec. contractility
    • Can become chronic and lead to dilated cardiomyopathy

This is an infection in the muscles of the heart, most commonly caused by the Coxsackie B virus that follows upon a respiratory or viral illness, bacteria and other infectious agents.

risk factor myocarditis
Risk factor-myocarditis
  • Hx of URI
  • Toxic or chemical effects(radiation, alcohol)
  • Autoimmune
  • Metabolic-lupus
  • Heat stroke or hypothermia
assessment myocarditis
Assessment myocarditis
  • Infection and CHF
    • Fatigue,DOE
    • Tachycardia
    • Arrhythmias
    • Chest pain- maybe an MI
    • Signs of CHF
diagnostic tests1
Diagnostic Tests
  • EKG- ST segment and T wave changes
  • CK-MB and Troponin may be elevated
  • Endomyocardial biopsy
  • Antibiotics
  • Antiviral with interferon-a
  • Corticosteroids or immunosuppressents
  • HF drugs-ACE, diuretics, beta blockers etc
  • Antiarrhythmics
  • Anticoagulants
other treatments
Other Treatments
  • Bedrest and activity restrictions
  • **Activities may be limited for 6 months- 1 yr.

GOAL- Decrease workload of the heart

nursing diagnoses1
Nursing Diagnoses
  • Activity Intolerance
  • Decreased CO
  • Anxiety
  • Excess fluid Volume

A 42 year old West African man was admitted unconscious to the intensive care unit, after an out of hospital cardiac arrest and resuscitation by a friend. He had little medical history of note other than that he had had a recent upper respiratory tract infection. There were no risk factors for HIV infection. While on intensive care he had recurrent episodes of ventricular fibrillation requiring multiple dc shocks, but ultimately settled on treatment with intravenous lignocaine (lidocaine), amiodarone, and overdrive pacing. His resting ECG showed non-specific T wave changes (fig 1) and he intermittently had non-sustained episodes of a broad complex, irregular tachycardia (fig 2). Full blood count, urea and electrolytes, and liver function tests were normal. Transthoracic echocardiography showed normal left ventricular function and size. He gradually recovered


without any sequelae. Electrophysiological testing revealed inducible non-sustained polymorphic ventricular tachycardia. Coronary angiography was entirely normal. A right ventricular biopsy was taken which subsequently showed healing myocarditis (fig 3). The patient declined to have an implantable cardioverter/defibrillator and was discharged on oral amiodarone.


Normal Pericardium

  • slit like opening between two layers
  • contains pericardial fluid
    • film of serous fluid
  • lubricant that reduces friction between the beating heart and pericardial sac
etiology pathophysiology2
  • Pericarditis
    • bacterial, fungal or viral infection
    • Heart loses natural lubrication(15-50cc’s)and layers roughen and rub
    • Inflammatory process causes lymphatic fluid build-up
    • Pericardial Effusion- usually 250 cc’s before show up on x-ray



Original heart size

Excess pericardial fluid

determination of pulsus paradoxus
Determination of Pulsus Paradoxus
    • Place the patient in a position of comfort and take their systolic blood pressure during baseline respiration.
    • Raise sphygmomanometer pressure until Korotkoff sounds disappear.
    • Lower pressure slowly until first Korotkoff sounds are heard during early expiration with their disappearance during inspiration
    • Record this pressure.
    • Very slowly lower pressure (1mm at atime) until Korotkoff sounds are heard throughout the respiratory cycle with even intensity.
    • Record this pressure.
    • The difference between the two recorded pressures is the Pulsus Paradox.
    • Hemodynamically significant pulsus paradox is greater than or equal to 10% of the pressure at which all Korotkoff sounds are heard with even intensity.
  • ______________________________________________________________________________________
risk factors pericarditis
Risk Factors/pericarditis
  • Post MI (Dressler’s syndrome)
  • Secondary to chemo and cancer
  • Secondary to uremia in renal failure-40-50% of ESRD Pts. Develop this
  • Trauma or cardiac surgery
  • Can be chronic disorder-pericardium becomes rigid
assessment pericarditis
Assessment pericarditis
  • Inflammation and pain
    • Friction rub-LLsternal border in knee chest position Cardiac Resources
    • Fever
    • Substernal, pleuritic chest pain
      • Inc. with coughing, breathing,turning,lying flat
      • Dec. with sitting up and leaning forward
diagnostic tests to r o
Diagnostic Tests- to R/O
  • CBC-inc. WBC and ESR
  • Cardiac Enzymes- inc. but not as much as with MI
  • EKG
  • Echo- for wall movement
  • CXR
  • CT or MRI- for pericardial effusion
  • ASA or tylenol
  • Corticosteroids
surgical invasive interventions for all
Surgical/invasive Interventions for all
  • Pericardiocentesis
    • Hook needle to V lead
    • Look for ST elevation
    • Withdraw fluid
    • Afterward watch for cardiac tamponade(PP)

Valve Replacement

Heart Transplant

Pericardial window


A procedure in which an opening is made in the pericardium to drain fluid that has accumulated around the heart. A pericardial window can be made via a small incision below the end of the breastbone (sternum) or via a small incision between the ribs on the left side of the chest.

nursing diagnoses for pericarditis
Nursing Diagnoses for Pericarditis
  • Acute Pain
  • Ineffective Breathing Pattern
  • Risk for Decreased Cardiac Output
  • Activity Intolerance
specific nursing assessment
Specific Nursing Assessment
  • Paradoxical pulse
  • Murmur
  • Pericardial rub
  • Emboli
  • Chest pain
  • CHF
comfort measures
Comfort Measures
  • O2
  • Bedrest
  • Positioning
  • Space Activities
  • Prevent complications of immobility
  • Psychological support
case studies
Case Studies
  • myocarditis
  • Vascular Infections Case 7-endocarditis

Johns Hopkins Arthritis Case report on rheumatoid pericarditis