A 45-year-old male presents to the local Emergency Department with complaints of moderate to severe chest pain, with radiation to the neck-shoulder region. The patient denies any personal history of heart disease, but reports that his father passed away from a heart attack at the age of 69. Temperature = 102 F. Pulse = 110. Respiratory rate = 25. Blood pressure = 100/63.

The head, ear, nose, and throat exam is unremarkable. During pulmonary auscultation, the patient states that pain gets much worse every time he is asked to take a deep breath. A triphasic grating sound is heard during cardiac auscultation. The patient refuses to lie down for the abdominal exam, saying that the pain gets too bad when he is supine. An EKG is ordered, and shows ST elevation in all leads except for V1 and aVR. PR depression is noted. Troponin I is mildly elevated.

1. Which of the following conditions constitutes the most likely diagnosis in this patients case?A. myocardial infarction B. Dresslers syndrome C. pericarditis D. hypertrophic subaortic stenosis E. cardiac tampanode2. Which of the following methods represents the most appropriate next diagnostic step in working up this patients condition?A. angiography B. CT scan C. technetium-99 perfusion scan D. magnetic resonance imaging E. echocardiography

3. Which of the following represents the most appropriate treatment in the management of this patient?A. non-steroidal inflammatory drugs B. cardiac catheterization with angioplasty C. coronary artery bypass graft procedure D. emergent IV administration of heparin E. pericardiocentesis

ANSWER KEY:1. C 2. E 3. A

Pericarditis endocarditis myocarditisS.Ajitha Rani IInd yr M.sc Nursing

IntroductionInfection and inflammation of the heart have multiple tiologies.. The disease can cause permanent damage to structures of the heart with long term cardiac disability.

LAYERS OF THE HEART

PericardiumTwo layers - composed of fibrous tissueinner visceral layer, attached to epicardiumouter parietal layerstabilizes heart in anatomic positionprotects heart - (contact with surrounding structures)

PericardiumCan be a primary site of diseaseinvolved in other disease processes that affect the heartaffected by other diseases of adjacent tissue

Acute PericarditisAcute inflammation of the pericardiumOrigininfectious,systemic diseases,malignancy, radiation,drug toxicity,hemopericardium,other inflammatory processes in the myocardium or lungPathologic process often involves both the pericardium and the myocardium

Causesviral infection most common coxsackievirus, & echovirusalso- HIV,influenza,Epstein-Bar, varicella, hepatitis, mumpsbacterial infectionstaphylococcus, Strep pneumoniae, B-hemolytic streptococci, Mycobacterium tuberculosis, lyme dzFungal infectionMalignancy

PATHOPHYSIOLOGY

Due to etiological factors Begins in acute pericarditis with pericardial effusionEffusion slowly progresses to the subacute phase of reabsorption followed by chronic inflammation

FIBROSIS SCARRINGTHICKENING OF THE PERICARDIUM

Closure of pericardial spaceFusion of the layers

Rigidity & Inelasticty which reduces the filling of heart chambers

Decreased cardiac output HEART FAILURE

Subjective symptomsSharp pain over the sternum, radiating to the back, neck, shoulders and armsPain increases with deep inspirationMay be relieved by sitting upDifficulty breathingTachycardiaFeeling of fullness in the chest

Diagnostic tests

HistoryWBCESRCardiac enzymesEKG may show ST elevationCK-MB may be elevatedBUNEchocardiogram

Nursing interventions

Assess pain and give RXHOB elevated for dyspneaBedrest to decrease workload of the heartO2 as orderedMonitor Vitals including CVP

Viral PericarditisMost commonly caused by coxsackievirus, & echovirusCan also be caused by HIV, influenza, Epstein-Bar, varicella, hepatitis, mumpsMost commonly affects males < age 5

Viral Pericarditis- TreatmentGenerally symptomatic Txaspirin or NSAIDsCorticosteroids -(unresponsive cases)Symptoms generally subside over several days to weeksMay be recurrences - during first few weeks - months

Bacterial Pericarditisstaphylococcus, Strep, pneumoniae, B-hemolytic streptococci, Mycobacterium tuberculosisUsually direct result from pulmonary infectionpatients often present in a critically ill stateBorrelia burgdorferi (Lyme Disease organism) can also cause myopericarditis

Tuberculous PericarditisRare in developed countries - common elsewhereResults from direct lymphatic or hematogenous spreadcommonly have associated pleural effusions & small to moderate pericardial effusionssubacute presentation/non-specific symptoms (fever, night sweats, fatigue)

Uremic PericarditisComplication of renal failureOccurs in untreated uremia and in stable dialysis patientsPresents with or w/o symptoms, typically afebriletamponade is commonusually resolves with institution or more aggressive dialysis

Contd.pericardiectomy may become necessaryIndomethacin & systemic glucocorticoids ineffective for uremic pericarditis

Neoplastic pericarditisCommonly caused by breast and renal cell carcinoma, Hodgkin's Disease and lymphomasneoplastic processes involving the pericardium are the most common cause of pericardial tamponade in many countriesMRI/CT

Contd..Prognosis poor - only small minority survive >yearEffusion can be drained, chemotherapeutic agents or tetracycline may prevent recurrencepartial pericardiectomy from a subxiphoid incision may be successful

Radiation PericarditisUsually occurs within the first year after exposure but can be delayed for many yearsSymptomatic therapy - initial approach but recurrent effusions and constriction require surgery

Constrictive PericarditisConstriction occurs when fibrous thickening and loss of elasticity of the pericardium results in interference of diastolic filling usually following inflammation

DiagnosisECG - may show low voltage QRS complexes and inverted T wavesChest x-ray - 50% of cases show pericardial calcificationDoppler echocardiographyCardiac CT, MRIConsider other diseases - acute pericarditis, myocarditis, exacerbation of chronic ventricular dysfunction, or systemic process (eg sepsis)

TreatmentDRUG THERAPY:Antibiotics: penicillin, penicillin G & anti tuberculosis chemo therapyAntifungalAntimicrobial ageColchicines & indomethacin for those who cant tolerate NSAIDsHigh dose salicylatescorticosteroids

SURGICAL MANAGEMENT:

Pericardiocentesis: a percutaneous approach guided by ECG & echocardiogram.Needle inserted into the pericardial space to remove fluid for analysis and to relieve cardiac pressure.PercardiectomyPartialTotalComplete or partial resection of the pericardium through a median sternotomy with use of cardiopulmonary bypass.

Endocarditis Infective endocarditis is defined as an infection of the endocardial surface of the heart, which may include one or more heart valves, the mural endocardium, or a septal defect

INFECTIVE ENDOCARDITIS

Increased mortality rates are associated with increased age, infection involving the aortic valve, development of congestive heart failure, central nervous system (CNS) complications, and underlying diseaseAffects men more than women (2:1 ratio)Affects all age groups - however, 50% of cases in adults over age 50

Predisposing factorsCARDIAC CONDITIONS

NON CARDIAC CONDITIONS

PROCEDURE ASSOCIATED RISKS

HEART WITH INFECTIVE ENDOCARDITIS

Pathophysiology:

Damage to epithelial surface & valves.Formation of vegetation.Embolization.Sepsis, heart failure & block.

NON SPECIFIC MANIFESTATION:

Low grade feverArthralgiasMyalgiasBack pain and headacheClubbing of fingersAbdominal discomfort

VASCULAR MANIFESTATIONSSplincter hemorrhagePetechiaeOslers nodesJane ways lesionsRoths spotMurmers & tachycardiaEmbolization of the spleen, kidney, brain, lungs and vessels.Abdomen- acute melena pain.

Splinter hemorrhages(Panel A) are normally seen under the fingernails. They are usually linear and red for the first two to three days and brownish thereafter. Panel B shows conjunctival petechiae. Osler's nodes (Panel C)are tender, subcutaneous nodules, often in the pulp of the digits or the thenar eminence. Janeway's lesions (Panel D) are nontender, erythematous, hemorrhagic, or pustular lesions, often on the palms or soles

Diagnostic studiesBaseline studies, such as a complete blood count (CBC), electrolytes, creatinine, BUN, glucose, and coagulation panelBlood cultures: Two sets of cultures have >90% sensitivity when bacteremia is present. Three sets of cultures improve sensitivity and may be useful when antibiotics have been administered previously

TreatmentMEDICAL MANAGEMENT:ANTIBIOTIC THERAPY : Pencillin is the drug of choice. In fungal endocarditis : AmphotericinB and FungisomeClindamycin is the drug of choice for patient with penicillin.Ampicillin, ceftriaxone, vancomycin, amoxicillin and nafcillin.Azithromycin, cefazolin, cephalaxin and clarithromycin

American heart association treatment Administer penicillin G at 12-18 million U/d IV by continuous pump or in 6 equally divided doses for 4 weeksAdminister ceftriaxone at 2 g/d IV for 4 weeks. It may be given intramuscularly (IM) for short periods if venous access problems develop; ceftriaxone allows once-a-day outpatient IV therapy for clinically stable patients.

Contd.Administer penicillin G and gentamicin at 1 mg/kg (based on ideal body weight) every 8 hours for 2 weeks; short-course therapy with ceftriaxone and gentamicin for 2 weeks is a cost-effective regimen and is effective in selected patients; short-course therapy is recommended for those with uncomplicated NVE caused by sensitiveS viridansand of less than 3 months duration

Contd..In patients who are allergic to penicillin, use vancomycin at 30 mg/kg/d IV in 2 equally divided doses for 4 weeks; the vancomycin dose should not exceed 2 g/d unless serum levels are monitored and can be adjusted to attain a peak vancomycin level of 30-45 mcg/mL 1 hour after completion of the intravenous infusion of vancomycin

Contd.Complete bed restRepeating culturesNutritional supplementsClose follow upPatient with prosthetic valve require caution anticoagulation because anticoagulant therapy does not reduce the risk of Embolization and have intracerebral hemorrhage risk

SURGICAL MANAGEMENT:Debridement of vegetationClosure of fistulaExcision and replacementDrainage of abscess

NURSING MANAGEMENT:

Normal or baseline cardiac functionsPerformance of ADLKnowledge of therapeutic regimen Maintaining Adequate cardiac output & tissue perfusion

COMPLICATION:CNS is a most frequently ravaged by systemic emboli between 60% & 70% often middle cerebral arteryCVA- appearance of symptoms like lethargy, confusion, paralysis fever & blindness.Intracranial mycotic aneurysm formation in septic emboli: it represents the spread of infection to the arterial intraluminal space & extension through intima & vessel cells

Myocarditis

MyocarditisInflammation of the myocardium May be the result of systemic disorder or infectious agent ...usually follows an upper resp infectionPericarditis frequently accompanies myocarditisDrug induced, cytotoxic agents,also, cocaine

CausesBacterial causes include;Corynebacterium diphtheriae, Neisseria meningitides, Mycoplasma pneumoniae, and B-hemolytic streptococciViral etiologies include;coxsackie B, echovirus, influenza, parainfluenza, Epstein-Barr, and HIV

PHASES OF MYOCARDITIS:

Acute phaseSubacute phaseChronic phase

ACUTE MYOCARDITIS (0-3 days)Viral infectionMyocyte damageMyocyte antigens releasedCytokines releasedSUBACUTE MYOCARDITIS (4-14 DAYS)Infiltrating mononuclear cellsCytokine productionT & B lymphocytes activatedNeutralizing antibodiesViral clearance CHRONIC PHASE (15-90 DAYS)Fibrosis & cardiac enlargement

Clinical featuresFever with tachycardiaFatigue & malaiseMyalgiasNausea & vomitingPalpitationsDyspneaPharyngitislymphadenopathy

DiagnosisNonspecific ECG changes, atrioventricular block, prolonged QRS duration, or ST segment elevation (in cases of accompanying pericarditis) normal chest x-raycardiac enzymes may be elevatedDifferential diagnosis includes cardiac ischemia or infarction, valvular disease and sepsis

MANAGEMENT:DIGOXIN: to improve myocardial contractility & reduces ventricular rateDIURETICS: reduce fluid volume & decrease preloadAntidysarhythmic therapy: Quinidine & procainamideNo hypotension to give nitroprusside

Beta blockers & amiodaroneTo reduce after load & improve cardiac output by reducing systemic arterial resistanceImmunosuppresive therapy:Prednisolone, azathioprine & cyclosporineIntravenous immunoglobulin : increase left ventricular function and improves survival rate.Antiviral agents: ribovarin & alpha interferon

Oxygen therapy Bed restRestricted activityCombination therapy:CyclosporineMuromonab- CD3CorticosteroidsAzathioprine

NURSING MANAGEMENTTo decrease the myocardial workloadFocused upon symptomatic reliefRecord vital signs observe very keenlyManagement of fluid balanceUse fowlers positionSpacing of activityProvision for quite environmentReducing fatigueEducate patient & family members

Heart failure & cardiomyopathy

Nursing DiagnosisDecreased cardiac output related to structural changesIneffective tissue perfusion related to interruption of blood flow.Hyperthermia related to infectionImbalanced nutrition less than body requirement related to anorexia.Activity intolerence related to generalized weaknessPain related to inflammation.Anxiety related to acute illnessDeficient knowledge related to lack of experience & information of disease.

REFERENCESBlack,J.M.&Jacobs,E.(1998).Medical and surgical nursing Clinical management for continuity of care (5th ed) Philadelphia: W.B Saunders.Lewis,S.L.Heitkemper,M.Dirksen,S.R.et al.(2007).Medical surgical nursing assessment and management of clinical problems(7thed).Missouri. Mosby elsevier publishers.Smeltzer,S.C.(2004).Brunner & suddarths textbook of medical surgical nursing (10 th ed) Philadelphia : Lippincott Williams & Wilkins publishers.

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