The inflammation of the heart muscles, such as myocarditis, the membrane sac which surrounds the heart called as pericarditis, and the inner lining of the heart or the myocardium, heart muscle as endocarditis are known as the inflammatory heart diseases.

1. BY RAJEE RAVINDRAN

2. WELCOME

3. INFLAMMATORY DISEASES OF HEART
The inflammation of the heart muscles,
the membrane sac which surrounds the
heart, or the inner lining of the heart
are known as the inflammatory heart
diseases.

6. PERICARDITIS
TYPES
ACUTE
PERICARDITIS
CHRONIC
PERICARDITIS
CAUSES
INFECTION
NON
INFECTION
VIRAL
BACTERIAL
FUNGAL
TB
HIV
UREMIA
RADIATION
INDUCED
CANCER
TRAUMA
TO HEART
MEDICATION
SIDE EFFECTS

7. PATHOPHYSIOLOGY OF PERICARDITIS
INFECTION ETIOLOGY NON INFECTION ETIOLOGY
INFLAMMATORY RESPONSE
INFLUX OF NEUTROPHILS + OTHER CHEMICAL MEDIATORS
CHANGE IN THE PERMEABILITY OF PERICARDIAL VASCULARITY
PERICARDIAL INFLAMMATION AND EDEMA
RESTRICTION
OF HEART
MOVEMENT
CHEST
PAIN

8. CLINICAL MANIFESTATIONS
ACUTE PERICARDITIS CHRONIC PERICARDITIS

9. DIAGNOSIS OF PERICARDITIS
• MEDICAL HISTORY AND PHYSICAL EXAM
• ECG
• ECHO
• CARDIAC CT/ MRI
• DOPPLER IMAGING
• BLOOD TEST – CRP, BUN, TROPONIN-I, CK-MB, MYOGLOBIN, ESR

10. MANAGEMENT
MEDICAL
NON-
PHARMACOLOGICAL
SURGICAL
ANTIBIOTIC
ANTIFUNGAL
NSAID
DIURETICS
ANTIPYRETICS
ANALGESICS
PERICARDIOCENTESIS
HAEMODIALYSIS
PERICARDIECTOMY

11. COMPLICATIONS OF PERICARDITIS

12. MYOCARDITIS
TYPES
LIEBERMAN’S
CLINICOPATHOLOGICAL
PATHOLOGICAL ETIOLOGICAL
 FULMINANT
MYOCARDITIS
 ACUTE MYOCARDITIS
 CHRONIC ACTIVE
MYOCARDITIS
 CHRONIC
PERSISTENT
MYOCARDITIS
 LYMPHOCYTIC
 EOSINOPHILIC
 GRANULOMATOUS
 NEUTROPHILIC
 REPERFUSION
 INFECTIOUS
 POST VIRAL
AUTOIMMUNE
MEDIATED
 AUTOIMMUNE
MEDIATED
 DRUG ASSOCIATED

13. CAUSES OF MYOCARDITIS
INFECTIONS TOXINS IMMUNOLOGIC
VIRAL
PROTOZOAN
BACTERIAL
FUNGAL
PARASITIC
ALCOHOL
CARBON
MONOXIDE
SNAKE VENOM
DRUGS
(ANTIPSYCHOTIC
SUCH AS
CLOZAPINE)
ALLERGIC
REJECTION AFTER
A HEART
TRANSPLANT
AUTOANTIGENS
HEAVY METALS
PHYSICAL AGENTS

14. PATHOPHYSIOLOGY OF MYOCARDITIS
CLINICAL MANIFESTATIONS OF MYOCARDITIS
CHEST PAIN
PALPITATIONS
FEVER
SHORTNESS OF BREATH

15. DIAGNOSIS OF MYOCARDITIS
• ECG –
• Elevated C-reactive protein (CRP)
• Elevated erythrocyte sedimentation rate (ESR),
• Increased IgM (serology) against viruses known to affect the myocardium.
• Markers of myocardial damage (troponin or creatine kinase cardiac
isoenzymes) are elevated.
• Biopsy Focal destruction of myocytes explains the myocardial pump failure.
• Cardiac magnetic resonance imaging (cMRI or CMR) in diagnosing
myocarditis by visualizing markers for inflammation of the myocardium

16. MANAGEMENT OF MYOCARDITIS
MEDICAL SURGICAL
DIGOXIN
DIURETICS
INOTROPES
INTRAVENOUS
IMMUNOGLOBULINS
SYSTEMIC
CORTICOSTEROIDS
HEART
TRANSPLANTATION
EXTRA CORPOREAL
MEMBRANE
OXYGENATION

17. COMPLICATIONS OF MYOCARDITIS

18. ENDOCARDITIS
TYPES
INFECTIVE
ENDOCARDITIS
NON INFECTIVE
ENDOCARDITIS
ACUTE INFECTIVE
ENDOCARDITIS
SUBACUTE
ENDOCARDITIS

19. CAUSES OF ENDOCARDITIS
• BACTERIA
• FUNGI
• VIRUSES
• CARDIAC CONDITIONS(PROSTHETIC VALVES, CARDIAC LESIONS)
• NON CARDIAC CONDITIONS (NOSOCOMIAL BACTEREMIA)
• PROCEDURE ASSOCIATED RISKS(DENTAL PROCEDURES,RECENT HEART
SURGERIES)
• INTRAVASCULAR DEVICES(CVC,HEMODYNAMIC MONITORING)

20. PATHOPHYSIOLOGY OF ENDOCARDITIS
ANATOMIC OR
TRAUMATIC CHANGES
DAMAGE TO ENDOTHELIAL SURFACE
ADHERENCE OF CAUSATIVE FACTOR TO VALVE SURFACE
FORMATION OF VEGETATIONS ON VALVE SURFACE
LEFT SIDE HEART
EMBOLIZATIONS
LOCAL VALVE
DAMAGE
RIGHT SIDE HEART
EMBOLIZATIONS
BRAIN, LIMB
KIDNEY, LIVER
SPLEEN
SEPSIS
HEART FAILURE
HEART BLOCK
LUNGS

22. CLINICAL MANIFESTATIONS OF ENDOCARDITIS
ACUTE INFECTIVE ENDOCARDITIS SUBACUTE INFECTIVE ENDOCARDITIS
ONSET sudden gradual
USUAL
ORGANISM
Staphylococcus aureus Streptococcus viridans, enterococci, gram-
negative
and gram-positive bacilli, fungi, yeasts
RISK FACTORS Usually occurs in previously normal
heart; intravenous
drug use, infected intravenous sites
Usually occurs in damaged or deformed
dental work,
invasive procedures, and infections
PATHOLOGICAL
PROCESS
Rapid valve destruction Valve destruction leading to regurgitation;
embolization
of friable vegetations
PRESENTATION Abrupt onset with spiking fever and
chills,
manifestations
of heart failure
Gradual onset of febrile illness with cough,
dyspnea,
arthralgias,
abdominal pain

23. CLINICAL MANIFESTATIONS OF ENDOCARDITIS
PERIPHERAL MANIFESTATIONS INCLUDE
PETECHIAE
SPLINTER
HEMORRHAGE
OSLER’S NODES
JANEWAY LESIONS
ROTH’S SPOTS

24. DIAGNOSIS OF ENDOCARDITIS
BLOOD CULTURES
ECG
ECHO
SEROLOGIC IMMUNE TESTING
CBC,ESR
CHEST XRAY

25. MANAGEMENT OF ENDOCARDITIS
MEDICAL SURGICAL
ANTIBIOTICS
REPLACE SEVERLY
DAMAGED VALVES
REMOVE LARGE
VEGETATIONS

26. NURSING MANAGEMENT OF ENDOCARDITIS
Interventions
• Auscultate apical pulse, assess heart rate, rhythm.
• Inspect skin for pallor, cyanosis
• Palpate peripheral pulses and monitor BP
• Encourage rest, semi recumbent in bed or chair. Assist with physical care as
indicated.
• Provide quiet environment: explain therapeutic management, help patient
avoid stressful situations, listen and respond to expressions of feelings.
• Elevate legs, avoiding pressure under knee.
• Encourage active and passive exercises. Increase activity as tolerated.
• Check for calf tenderness, diminished pedal pulses, swelling, local redness, or
pallor of extremity.
Decreased cardiac output related to structural changes evidenced by tachycardia,
dysrhythmias, ECG changes, chest Pain.

27. NURSING MANAGEMENT OF ENDOCARDITIS
Interventions
• Check vital signs before and immediately after activity
• Document cardiopulmonary response to activity. Note tachycardia,
dysrhythmias, dyspnea, diaphoresis, pallor.
• Evaluate accelerating activity intolerance.
• Provide assistance with self-care activities as indicated.
• Assist patient with ROM exercises. Check regularly for calf pain and
tenderness.
Activity intolerance related to imbalance between oxygen supply/demand evidenced
by Weakness, fatigue, changes in vital signs, presence of dysrhythmias dyspnea, pallor,
diaphoresis

28. NURSING MANAGEMENT OF ENDOCARDITIS
Interventions
• Assess patient pain for intensity using a pain rating scale, for location and for
precipitating factor Administer or assist with self-administration of vasodilators, as
ordered.
• Assess the response to medications every 5 minutes.
• Establish a quiet environment.
• Elevate head of bed.
• Monitor vital signs, especially pulse and blood pressure, every 5 minutes until pain
subsides.
• Provide oxygen and monitor oxygen saturation via pulse oximetry, as ordered.
• Teach patient relaxation techniques and how to use them to reduce stress.
• Instruct patient on eating a small frequent feeding
Ineffective tissue perfusion related to decreased cardiac output.

29. SUMMARY AND CONCLUSION

30. BIBLIOGRAPHY
Polaski L A, Tatra E S: Luckmann’s Core Principles and Practice of
Medical Surgical Nursing, Elsevier (2010), p 736-744
Smeltzer C S, Bare G B, Hinkle L J, Cheever H K : Brunner and
Suddarth’s Textbook of Medical Surgical Nursing: 11th edition, vol 1
(2009), p933-942
Lewis L S, Heitkemper M M et al: Chintamani- Lewis’s Medical Surgical
Nursing. Mosby. 7th edition(2011), p 860-869
Lemane P, Burke K, Medical Surgical Nursing, 4th edition, p1045-1051

31. EVALUATION