inflammatory disorders of the heart

Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

Inflammatory Disorders of the Heart

EndocarditisPericarditisMyocarditis

infection of endocardial surface of heart

focal or diffuse inflammation of myocardium

inflammation of pericardial sac (pericardium)

http://yourtotalhealth.ivillage.com/heart-injuries-infections

http://www.heartpoint.com/endocarditis.html

http://yourtotalhealth.ivillage.com/pericarditis.html

http://yourtotalhealth.ivillage.com/myocarditis.html


Endocarditis: precipitated by bacteria/fungal infection; potential death from emboli and valvular disturbance

Myocarditis: virus, toxin or autoimmune response damage heart muscle > lead to cardiomyopathy and death!

Pericarditis: Bacterial, fungal or viral infection affect visceral and parietal pericardium; restrict heart pumping action> lead to cardiac tamponade and death!


Layers of the Heart

Fig. 37-1Fig. 37-1

Layers of heart muscle and pericardium; section of heart wall shows fibrous pericardium, parietal and visceral layers of serous pericardium (with pericardial sac between them), myocardium, and endocardium-


Layers of the Heart Muscle


TISSUES SURROUNDING THE HEART


Infective Endocarditis (Click to access YOUTube video)

Infection of inner layer of heart- usually affects cardiac valves

Was almost always fatal until development of penicillin

15,000 cases diagnosed in US each year

http://www.youtube.com/watch?v=V_G5qqv7Oqc


A- Aortic ValveB- Mitral ValveC- Tricuspid Valve - Pulmonary Valve


A&P Review-

After entering left atrium via pulmonary veins, blood moves through the _____ into left ventricle.

Finally, it travels through the _____ and out of heart

A- Aortic ValveB- Mitral ValveC- Pulmonary ValveD- Tricuspid Valve

Blood enters right atrium and moves through _______ into right ventricle.Blood then moves from right ventricle into pulmonary artery via _________.

A- Aortic ValveB- Mitral ValveC- Pulmonary ValveD- Tricuspid Valve


Risk Factors- endocarditis Hx of rheumatic fever or damaged heart

valve Prior history of endocarditis Invasive procedures- (introduce bacteria into

blood stream) dental,gyne, etc. Recent Dental Surgery Permanent Central Venous Access IV drug users Valve replacements


Classification Subacute form (subacute bacterial endocarditis-SBE)

Gradual onset; longer clinical course Caused by enterococci Usually those with damaged valves

Acute form Shorter clinical course Abrupt onset Usually those with healthy valves Usually caused by staph aureus

*Classify by cause as IVBA; prosthetic valve endocarditis (PVE), fungal endocarditis


Causative Organisms Most common causative organism

Streptococcus viridans Staphylococcus aureus Viruses Fungi


Etiology and Pathophysiology Key -Blood turbulence within heart

allows causative agent to infect previously damaged valves or other endothelial surfaces

Principal risk factors Prior endocarditis Prosthetic valves Acquired valvular disease Cardiac lesions


When valve damaged, blood > slowed down > forms clot.

Bacteria > into blood stream Bacterial or fungal vegetative growths

deposit on normal or abnormal heart valves

Infection of innermost layers of heart may occur in people with: congenital and valvular heart disease history of rheumatic heart disease normal valves with increased amounts of bacteria


Endocarditis

http://www.heartpoint.com/endocarditis.html


Bacterial Endocarditis of Mitral Valve

Bacterial endocarditis of mitral valve. Valve covered with large, irregular vegetations (note arrow). From text


Any valve can be affected!


Etiology and Pathophysiology Vegetation

Fibrin, leukocytes, platelets, and microbes

Adhere to valve or endocardium Embolization of portions of vegetation

into circulation


Sequence of Events in Infective Endocarditis (view carefully)

Fig. 37-3Fig. 37-3


Clinical Manifestations Nonspecific *Fever in 90% of patients Chills Weakness Malaise Fatigue Anorexia *Murmur


Clinical Manifestations Subacute form

Arthralgias Myalgias Back pain Abdominal discomfort Weight loss Headache Clubbing of fingers


Clinical Manifestations Vascular manifestations

Splinter hemorrhages in nail beds Petechiae * most common Osler’s nodes on fingers or toes *painful Janeway’s lesions on palms or soles Roth’s spots

*Murmur in most patients Heart failure in up to 80% with aortic valve

endocarditis *Manifestations secondary to embolism


Sites of emboli due to infective endocarditis (AKA metastic infections)-site determined by location of original lesion


Osler’s nodes

Splinter hemorrhages Roth spots

Janeway lesions


•Osler’s nodes- painful, red or purple pea-sized lesions on toes and fingertips

•Splinter hemorrhages- black longitudinal streaks on nail beds

•Janeway lesions- flat, painless, small, red spots on palms and soles

•Roth spots- hemorrhagic retinal lesions

http://en.wikipedia.org/wiki/Osler's_node

http://usmlemd.wordpress.com/2008/06/27/osler-nodes-vs-janeway-lesions-2/

http://en.wikipedia.org/wiki/Roth's_spot


Diagnostic Studies History

Recent dental, urologic, surgical, or gynecological procedures

Heart disease; onset *new heart murmur Recent cardiac catheterization Skin, respiratory, or urinary tract infection

Laboratory tests Blood cultures (if temp above 101, typically do 2 sets) WBC with differential ESR, CRP

Echocardiography- TEE best- see vegetations Chest x-ray 1) Vegetations on mitral valve

2) Vegetations on aortic Valce

http://video.google.com/videoplay?docid=-1965222768995270930&q=mitral+valve&total=101&start=30&num=10&so=0&type=search&plindex=0

http://www.youtube.com/watch?v=5pTCS6J51tE


Collaborative Care Prophylactic treatment for patients having

(see prevention) Removal or drainage of infected tissue Renal dialysis Ventriculoatrial shunts

Antibiotic administration Monitor antibiotic serum levels (peak &

trough) Subsequent blood cultures Renal function monitored

BUN, Creatinine


Collaborative Care Antibiotic therapy cont

IV for 2-8 weeks *Maybe oral meds if not good candidate for

IV and can identify and treat specific causative organism

Fungal and prosthetic valve endocarditis Responds poorly to antibiotics Valve replacement- adjunct procedure

Fever Comfort with ASA, Ibuprofen etc


Collaborative Care Surgical/Therapeutic/Nursing

Early valve replacement. Complete bed rest –only if temp remains

elevated or signs HF

Overall goals normal or baseline cardiac function performance of activities of daily living

(ADLs) without fatigue Antibiotic therapy cont


Nursing Diagnoses Risk for Imbalanced Body

Temperature-Hyperthermia Risk for Ineffective Tissue Perfusion-

emboli Risk for decreased cardiac output Ineffective Health Maintenance Deficient knowledge


Complications Emboli (50% incidence)

Right side- pulmonary emboli (esp. with IV drug abuse- Why??)

Left side-brain, spleen, heart, limbs,etc CHF-check edema, rales, VS Arrhythmias- A-fib Death

.


Collaborative Care Priority Teaching

Signs/symptoms of life-threatening complications of IE, as cerebral emboli, HF etc.

Monitor fever (chronic or intermittent)- sign that drug therapy ineffective

Monitor lab data, blood cultures- determine effectiveness of antibiotic therapy

*Critical-prophylactic antibiotic therapy prior to ANY invasive procedure - see later slide)


Collaborative Care Priority Teaching/nursing care

Stress need to avoid infectious people Avoidance of stress and fatigue Manage rest, hygiene, nutrition Assessment of nonspecific manifestations Monitor laboratory data Monitor patency of IV Teach reduction measures dec risk infection Stress follow-up care


Collaborative Care TABLE 37-3 SITUATIONS SeeREQUIRING ANTIBIOTIC PROPHYLAXIS TO PREVENT ENDOCARDITIS

Oral Dental manipulation involving

or periapical region of teeth Dental manipulation involving

perforation of oral mucosa Dental extractions/dental

implants Prophylactic teeth cleaning

with anticipated bleeding Respiratory

Respiratory tract incisions (e.g., biopsy)

Tonsillectomy/adenoidect GI/GU

Presence wound infection Presence UTI

•Eliminate risk factors•Patient teaching

•Penicillin prophylaxisRecent change Guidelines (not all require prophylaxis)• if prosthetic valve• History of endocarditis• Certain congenital heart defects• Heart transplant recipients-• Removal/drainageinfected tissue• Renal dialysis• Ventriculoatrial shunts

•*see tab 37-3&4

http://www.americanheart.org/presenter.jhtml?identifier=3047051


Risk Stratisfication for IEHigh Risk-

Mechanical prosthetic heart valve Natural prosthetic heart valve Prior infective endocardititis Valve repair with prosthetic material Most congenital heart diseases

Moderate Risk- Valve repair without prosthetic material Hypertrophic cardiomyopathy Mitral valve prolapse with regurgitation Acquired valvular dysfunction

Low Risk- Innocent heart murmurs Mitral valve prolapse without

regurgitation Coronary artery disease People with pacemakers/ defibrillators

• Prophylactic antibiotics are generally recommended only for people in the “High Risk” category


Pericarditis (Click to access YouTube video)

Pericarditis inflammation of pericardium, thin,

fluid-filled sac surrounding heart. Can cause severe chest pain especially

upon taking a deep breath) Shortness of breath; hear pericardial

friction rub.

http://www.youtube.com/watch?v=iXpP7Bju1jw


Etiology/Pathophysiology Pericarditis due to

Bacterial, fungal or viral infection infectious) Non-infectious as uremia Hypersensitive/autoimmune as Dresslers

syndrome Heart loses natural lubrication(10-15 ml

serous fluid); layers roughen and rub Inflammatory response>lymphatic fluid build-up- if sudden > cardiac tamponade- Pericardial Effusion- usually 250ml before show

on x-ray-Can have 1000ml (danger!)

http://en.wikipedia.org/wiki/Cardiac_tamponade

http://en.wikipedia.org/wiki/Pericardial_effusion


Pericardial Sac Anatomy-video

http://www.youtube.com/watch?v=bbvFAvDbYWk&feature=related


Fig. 37-4

Acute pericarditis. Note shaggy coat of fibers covering surface of heart.


Risk Factors/pericarditis Be Acute or Chronic Infectious, non-infections or

hypersensitive/autoimmune causes Acute-48=72 hrs post Mi or late-post MI

(Dressler’s syndrome)-4-6 wks Secondary to chemo and cancer Secondary to uremia in renal failure-40-

50% of pts will develop Trauma or cardiac surgery If chronic disorder-pericardium >rigid


Clinical Manifestations Inflammation and pain

Pericardial friction rub-(click to hear) diaphragm at LL sternal, lean forward, listen at inspiration

Fever Substernal, sharp, pleuritic chest pain

Inc. with coughing, breathing, turning, lying flat

Dec. with sitting up and leaning forward Referred to trapezius muscle Dyspnea

http://www.youtube.com/watch?v=44yL1oL4f_o


Complications of Pericarditis Pericardial Effusion

Cardiac Tamponade


Pericardial Effusion (YouTubeVideo)

Can occur rapidly or slowly Pulmonary compression-cough,

dyspnea, and tachypnea Phrenic nerve art sounds distant,

muffled *Slow build-up; no immediate effects;

if rapid>compression of heart >tamponade!

http://www.youtube.com/watch?v=zEJf6bz-OR0&feature=related


Cardiac Tamponade Compression of heart Occur acutely (trauma) or sub-acutely

(malignancy) Symptoms- chest pain, confusion, anxious,

^ CVP, restless, muffled heart sounds Later- tachypnea, tachycardia, and dec. CO,

NVD and pulsus paradoxus With slow onset dyspnea may be only

symptom If rapid compression-Medical Emergency

http://en.wikipedia.org/wiki/Cardiac_tamponade


PERICARDIUMCARDIAC TAMPONADE

Original heart size

Excess pericardial fluid


Cardiac tamponade

Physiology- Paradoxical pulse is a pulse that markedly decreases in amplitude during inspiration. On inspiration, more blood is pooled in the lungs and so decreases the return to the left side of the heart; this affects the consequent stroke volume.

Definition- a decrease in systolic BP with inspirations that is exaggerated in cardiac tamponade


Collaborative Care-Pericarditis, Pericardial Effusion,

Cardiac Tamponde

Diagnostic Tests Medications Surgical/Therapeutic Interventions Nursing Diagnosis/Interventions


Diagnostic Tests- to R/O CBC-inc. WBC, ESR, and CRP Cardiac Enzymes- inc. but not as much as

with MI *EKG- diffuse St elevation *important to

different from MI changes (acute pericarditis) Echo- for wall movement CXR; Doppler imaginga CT or MRI- for pericardial effusion Pericardiocentesis fluid- determine cause;

treat cardiac tamponade


Medications- ASA or tylenol NSAIDS *Corticosteroids Pain relief-HOB to 45 degrees, lean

forward Anti-anxiety meds; maybe proton

pump inhibitors


Surgical/invasive Interventions(remove fluid-treat tamponade)

Pericardiocentesis Hook needle to V lead- guided by EKG and

echo Look for ST elevation Withdraw fluid Afterward watch for cardiac tamponade

(PP), dysrhythmias, pneumothorax Pericardial window Percutaneous balloon pericardiotomy Sclerosing agent- tetracycline (Bonds layers

together)


Pericardiocentesis


Procedure in which opening is made in pericardium to drain fluid that has accumulated around heart-ericardial window can be made via a small incision below end of the breastbone (sternum) or via a small incision between the ribs on the left side of chest.See also Thoracoscopic Assisted Pericardial Window

Pericardial Window


Cardiac Tamponade and treatment

Live Search Videos: cardiac tamponade

Single-balloon percutaneous balloon pericardiotomy

Balloon creates a tear in wall of pericardium to insert a drain and instill local anesthesia

Technique used in managing patient with large pericardial effusions typically due to malignancy


Nursing Diagnoses for Pericarditis

Acute Pain Ineffective Breathing Pattern Risk for Decreased Cardiac Output Activity Intolerance


Nursing Management O2 (if indicated-as cardiac tamponade) Recognize complications Bedrest Positioning/sit up/lean forward Space Activities Prevent complications of immobility Psychological support Appropriate medication selection


Chronic Constrictive Pericarditis Starts with acute then scarring and

fibrosis occur See signs of HF and cor pulmonale;

most relate to dec. CO Most prominent finding is JVD and

pericardial knock (click to hear) Treatment of choice pericardectomy-

with use of cardiopulmonary bypass


Case Studies

John Hopkins- Rheumatoid Arthritis-Pericarditis Case study


MyocarditisMyocarditis-uncommon inflammation of

heart muscle (myocardium) . Can be caused by infectious agents,

toxins, drugs or for unknown reasons May be localized to one area of heart, or

affect entire heart. *Myocarditis (Click for YouTube video)


Etiology/Pathophysiology Virus, toxin or autoimmune response

causes necrosis of myocardium *Frequently caused by Coxsackie B virus Usually follows URI or viral illness-7-10 days Leads to dec cardiac contractility May become chronic *Lead to dilated cardiomyopathy and

require heart transplant or death


Myocarditis- infection in muscles of heart; most commonly caused by Coxsackie B virus that follows a respiratory or viral illness, bacteria and other infectious agents


Risk factor-myocarditis Hx of URI Toxic or chemical effects(radiation,

alcohol) Autoimmune disorders Post pericarditis Metabolic-lupus Heat stroke or hypothermia


Clinical Findings

Infection and CHF Fatigue, DOE Tachycardia, pleuritc chest pain Dysrhythmias- esp A fib Chest pain- maybe an MI Signs of HF *other late signs *Pericarditis frequently occurs with

myocarditis- check friction rub


Collaborative Care Diagnostic Tests Diagnostic Tests

EKG- ST segment and T wave changes-Why??

Leukocytosis, inc ESR, CRP troponin levels

CK-MB and Troponin may be elevated Endomyocardial biopsy- has risks; not

used for every case; is definitive Echo


Endomyocardial biopsy (Click for YouTube Heart Biopsy) *also helpful to understand cardiac tamponade


Medications Antibiotics Antiviral with interferon-a IVIG- experimental trials Corticosteroids or immunosuppressents *HF drugs- ACE, diuretics, beta blockers

etc Antiarrhythmics Anticoagulants- Why??


Other Treatments Bedrest and activity restrictions- Why

important?? **Activities may be limited for 6

months- 1 yr. O2

*GOAL- Decrease workload of heart to allow healing!


Nursing Diagnoses Activity Intolerance Decreased CO Anxiety Excess fluid Volume


Priority Question # 23 You have just received change of shift report about

these clients on coronary step-down unit. Who will you assess first?

A. 26 year old with heart failure caused by congenital mitral stenosis who is scheduled for balloon valvuloplasty later today.

B. 45 year old with constrictive cardiomyopathy who developed acute dyspnea and agitation about 1 hour before shift change.

C. 56 year old who had a coronary angioplasty and stent placement yesterday and has complained of occasional chest pain since the procedure.

D. 77 year old who transferred from intensive care 2 days ago after coronary artery bypass grafting and has a temperature of 100.6F.


Priority Question # 19

While working on the cardiac step-down unit, a nurse is precepting a new graduate RN who has been in a 6 week orientation program. Which client will be best to assign to the new GN?

A. 19 year old with rheumatic fever who needs discharge teaching prior to going home with a roommate today.

B. 33 year old admitted a week ago with endocarditis who will be receiving Ancef 2 gm IV.

C. 50 year old with newly diagnosed stable angina who has many questions about medications and nursing care.

D. 75 year old who has just been transferred to the unit after having coronary artery bypass grafting yesterday.

inflammatory disorders of the heart

Documents

affiliate of elsevier

cardiac tamponadecopyright

cardiac tamponade pp

large pericardial effusions

small incision

wall of pericardium

heartericardial window

ekg diffuse st elevation