Inflammatory Disorders

Inflammatory Disorders

Updated Spring 2012 by Nancy Jenkins

Layers of the Heart Muscle

TISSUES SURROUNDING THE HEART

Infective Endocarditis

• Infection of the inner layer of the heart

• Usually affects the cardiac valves

• Was almost always fatal until

development of penicillin

• Around 15,000 cases diagnosed

annually in the U.S.

Causative Organisms

Causative organism more virulent Streptococcus viridans Staphylococcus aureus Viruses Fungi

Etiology and Pathophysiology

Occurs when blood turbulence within heart allows causative agent to infect previously damaged valves (congenital or acqired valvular disease) or other endothelial surfaces

May occur in people with a history of rheumatic heart disease

May occur in people with normal valves with increased amounts of bacteria

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 Vegetation

– Fibrin, leukocytes, platelets, and microbes– Adhere to the valve or endocardium – Embolization of portions of vegetation into circulation

Classifications of Endocarditis

Acute Infective Endocarditis– Abrupt onset– Rapid course– Staph Aureus

Subacute Infective Endocarditis SBE- most common– Gradual onset– Systemic manifestations

Prosthetic Valve Endocarditis

Bacterial Endocarditis of the Mitral Value

Fig. 37-2Fig. 37-2

Sequence of Events in Infective Endocarditis

Fig. 37-3Fig. 37-3

Risk Factors- endocarditis

Hx of rheumatic fever or damaged heart valve Prior history of endocarditis Invasive procedures- (introduce bacteria into blood

stream) (surgery, dental, etc) Recent Dental Surgery Permanent Central Venous Access IV drug users Valve replacements

Nursing Assessment

Subjective Data– History of valvular, congenital, or syphilitic cardiac

disease– Previous endocarditis – Staph or strep infection– Immunosuppressive therapy-(HIV)– Recent surgeries and procedures

Nursing Assessment

Functional health patterns– IV drug abuse– Alcohol abuse– Weight changes– Chills

Nursing Assessment

– Diaphoresis– Fever– Bloody urine– Exercise intolerance – Generalized weakness– Fatigue – Cough

Nursing Assessment

– Dyspnea on exertion – Night sweats – Chest, back, abdominal pain

Collaborative Care

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

Assesment endocarditis

Infection and emboli– Emboli-spleen most often affected (splenectomy)– 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

– Murmur- 90% have murmurs Heart Sounds Assessment Video

– T above 101(blood cultures) and low-grade– Chills– Anorexia– Fatigue

Splinter hemorrhage

• small areas of bleeding under the fingernails or toenails.

• due to damage to capillaries by small clots

Janeway Lesions

• flat, painless red spots on palms and soles

Osler’s Nodes

Painful, pea-size, red or purple lesions On finger tips or toes

Roth spotsOsler’s nodes

Roth’s Spots

• hemorrhagic retinal lesions

Diagnostic Tests

Blood Cultures- Echocardiogram-TEE best- see vegetations Other- WBC with differential, CBC,ESR,

serum creatinine,CXR, and EKG

Echocardiogram-video

Mitral Valve involvement

Echocardiogram-

Diagnostic Criteria

Duke criteria 2 major

– Blood cultures and vegetations present

5 minor– symptoms

Treatment- Medications

Antibiotics– IV for 2-8 weeks– Monitor peaks and troughs of certain drugs– Monitor BUN and Creat.– Unclear success of oral antibiotics if not a good candidate

for IV. Oral antibiotics are considered when dealing with endocarditis:

– Of the tricuspid valve– With a causative organism sensitive to oral agents– Long-term IV therapy difficult or impossible– Outpatient f/u can be arranged

Nursing Diagnoses

Risk for Imbalanced Body Temperature Risk for Ineffective Tissue Perfusion-emboli Ineffective Health Maintenance

Complications

Emboli (50% incidence)– Right side- pulmonary emboli (esp. with IV drug abuse-

Why??)– Left side-brain, spleen, heart, limbs,etc

CHF- 80% incidence with involvement of aortic valve– check edema, crackles, VS

Arrhythmias- A-fib Death

.

Prevention

Eliminate risk factors Patient teaching

Risk Stratisfication for IE

High 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

Collaborative Care

Prophylactic treatment for patients having– Removal or drainage of infected tissue– Renal dialysis– Ventriculoatrial shunts– Dental, oral, or upper respiratory tract procedures

– Endocarditis video review

Video Review

Layers of the Heart Muscle

Myocarditis

Myocarditis is an uncommon inflammation of the heart muscle (myocardium). This inflammation can be caused by infectious agents, toxins, drugs or for unknown reasons. It may be localized to one area of the heart, or it may affect the entire heart.

(effects like pounding the heart get inflammation and swelling)

Etiology/Pathophysiology

Myocarditis-video– Virus, toxin or autoimmune response causes necrosis of the

myocardium– Most often caused by viral infection– Frequently caused by Coxsackie B virus– Frequently follows an upper respiratory infection or viral

illness– Get decreased contractility– Can become chronic and lead to dilated cardiomyopathy-

heart transplant or death

•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

Hx of upper respiratory infection Toxic or chemical effects (radiation, alcohol) Autoimmune or immunosuppresents- 10%

HIV develop it Metabolic-lupus Heat stroke or hypothermia

Assessment myocarditis

Infection and CHF– Fatigue,DOE– Tachycardia– Arrhythmias- PVCs, PACs, Atrial Tachycardias, – Chest pain– Signs of heart failure (S3, etc.)– Pericarditis frequently occurs with myocarditis-

check friction rub

Diagnostic Tests

EKG- Non-specific T-wave abnormalities CK-MB and Troponin may be elevated Endomyocardial biopsy- there are risks and not used

for every case but is definitive for myocarditis Chest X-Ray- Variable (Normal to Cardiomegaly) Echocardiogram Cardiovascular Magnetic Resonace A safe and sensitive noninvasive diagnostic test to

confirm the diagnosis is not available

Chest X-Ray in Myocarditis

Endomyocardial Biopsy (EMB)

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 the heart so it can heal

Nursing Diagnoses

Activity Intolerance Decreased CO Anxiety Excess fluid Volume

Pericarditis

Pericarditis is an inflammation of the pericardium, the thin, fluid-filled sac surrounding the heart. It can cause severe chest pain (especially upon taking a deep breath) and shortness of breath.

Pericardial Sac Anatomy-video

Etiology/Pathophysiology

Pericarditis– bacterial, fungal or viral infection– Heart loses natural lubrication(10-30cc’s) and

layers roughen and rub– Inflammatory process causes lymphatic fluid

build-up- if sudden may have cardiac tamponade– Pericardial Effusion- usually 250 cc’s before show

up on x-ray. Can have 1000cc’s.

Risk Factors/pericarditis

Post MI (Dressler’s syndrome) Radiation Infection Trauma Cancer Drugs and toxins Rheumatic diseases Trauma or cardiac surgery Can be chronic disorder-pericardium becomes rigid

Assessment pericarditis

Inflammation and pain– Pericardial friction rub- diaphragm at LL sternal border in knee chest position – 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

Diagnostic Tests- to R/O

CBC-inc. WBC, ESR, and CRP Cardiac Enzymes- elevated but not as much as with

MI EKG- ST elevation, PR changes Echo- for wall movement CXR CT or MRI- for pericardial effusion Pericardiocentesis fluid for analysis- attempt to

determine cause

ECG in Pericarditis

Medications

ASA or tylenol NSAIDS- ibuprofen Corticosteroids

Pericarditis video review Livestrong Pericarditis Video

Complications of Pericarditis

Pericardial Effusion- an accumulation of excess fluid in the pericardium

Cardiac Tamponade- an increase in intracardial pressure caused by pericardial effusion that results in compession of the heart

Pericardial Effusion-video

Can occur rapidly or slowly Pulmonary compression-cough, dyspnea,

and tachypnea Phrenic nerve involvement- hiccups Laryngeal nerve- hoarseness

Pericardial Effusion- EKGElectrical Alternans-video

Pericardial effusion with electrical alternans

•The QRS axis alternates between beats. In this example it is best seen in the chest leads where the QRS points in different directions!

•This is rarely seen and is due to the heart moving in the effusion.

Cardiac Tamponade-

Compression of the heart Can occur acutely (trauma) or sub-acutely

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

restless Later- tachypnea, tachycardia, and dec. CO, NVD

and pulsus paradoxus present With slow onset dyspnea may be only symptom

cardiac tamponade with aortic dissection

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

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 a time) 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 but we look at trends. People with COPD may have a paradox due to increased thoracic pressures.

Surgical/invasive Interventions

Pericardiocentesis-now use echo or fluoroscopy– Hook needle to V lead- guided by EKG and echo– Look for ST elevation– Withdraw fluid– Afterward watch for cardiac tamponade (PP), arrhythmias,

and pneumothorax

Pericardiectomy Pericardial window Sclerosing agent- tetracycline (Bonds layers

together)

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.

Pericardial Window

Cardiac Tamponade and treatment

Chronic Constrictive Pericarditis

Starts with acute then scarring and fibrosis occur

See signs of HF and cor pulmonale; most relate to decreased cardiac output

Most prominent finding is jugular vein distention (JVD)

Treatment of choice pericardectomy- with use of cardiopulmonary bypass

Nursing Diagnoses for Pericarditis

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

Review Specific Nursing Assessment for Inflammatory Heart Disorders

Paradoxical pulse Murmur Pericardial friction rub Emboli Chest pain CHF

Comfort Measures

O2 Bedrest Positioning Prevent complications of immobility Psychological support

Review- animations

Endocarditis

Myocarditis

Pericarditis

Case Study- Endocarditis

J.F. is a 50 year-old married homemaker with a genetic autoimmune deficiency; she has suffered from recurrent bacterial endocarditis. The most recent episodes were a Staphylococcus aureus infection of the mitral valve 16 months ago and a Streptococcus mutans infection of the aortic valve 1 month ago. During this latter hospitalization, an ECG showed moderate aortic stenosis, moderate aortic insufficiency, chronic valvular vegetations, and moderate left atrial enlargement. Two years ago J..F. received an 18-month course of TPN for malnutrition caused by idiopathic, relentless N/V. she has also had CAD for several years, and 2 years ago suffered an acute anterior wall MI. In addition, she has a history of chronic joint pain.

Now, after being home for only a week, J.F. has been readmitted to your floor with endocarditis, N/V, and renal failure. Since yesterday she has been vomiting and retching constantly; she also has had chills, fever, fatigue, joint pain, and headache. As you go through the admission process with her, you note that she wears glasses and has a dental bridge. She is immediately started on TPN at 125 ml/hr and on penicillin 2 million units IV q4h, to be continued for 4 weeks. Other medications are furosemide 80 mg PO qd, amlodipine 5 mg PO qd, K-Dur 40 mEq PO qd (dose adjusted according to laboratory results), metoprolol 25 mg PO bid, and prochlorperazine (Compazine) 2.5 to 5 mg IVP prn for N/V.

Admission VS are 152/48 (supine) and 100/40 (sitting), 116, 22, 37.9 degrees Celsius. When you assess her, you find a grade II/VI holosystolic murmur and a grade III/VI diastolic murmur; 2+ pitting tibial edema but no peripheral cyanosis; clear lungs; orientation x3 but drowsy; soft abdomen with slight left upper quadrant (LUQ) tenderness; hematuria; and multiple petechiae on skin of arms, legs, and chest.

What is going on?

Significance of orthostatic hypotension, wide pulse pressure and tachycardia?– Decreased cardiac output, aortic insufficiency

Significance of abdominal tenderness, hematuria, joint pain, and petechia?– Indicates embolization.

Clinical Manifestations in relation to J.F.

Primary manifestations– Fever – Chills – Weakness– Malaise– Fatigue – Anorexia– Arthralgia – Myalgia– Back pain– Abdominal discomfort– Weight loss– HA – Clubbing– Oslers Nodes– Janeway’s lesions – Petechiae

Secondary due to embolization

– LUQ pain – Splenomegaly– Local tenderness and

abdominal rigidity – Flank pain– Hematuria – Azotemia – *Gangrene– Hemiplegia– Ataxia– Aphasia– Visual changes– Change In level of consciousness– Pulmonary emboli (Right side)

What do J.F.’s lab values mean?

J.F.’s lab values: Na 138, K 3.9, Cl 103, BUN 85, Creatinine 3.9, glucose 185, WBC 6.7, Hct 27%, Hgb 9.0.

Her abnormal values and their indication?

Acute Viral Myocarditis

12/11/ 26 y/o wife, mother of two and student presented to a clinic with flu-like symptoms twice.

She received antibiotic and steroids with poor results. Two weeks later she presented to the Community

Memorial Hospital of Ventura emergency room where they treated her again with antibiotics, then discharged her.

Four days later, she presented back to the Ventura Emergency room with flu-like symptoms, shortness of breath, nausea and weakness, as well as, chest tightness upon physical exam.

Myocarditis cont.

She had elevated cardiac enzymes and was taken urgently to the cath-lab for a potential angioplasty.

Her cardiac catheterization showed that her coronary arteries were clean, however, her ejection fraction (EF) was <10%, with a cardiac output of 1.5 L/min.

Her blood pressure (BP) was 97/49 Echo showed severe left ventricle dysfunction. She was diagnosed with Acute Viral Myocarditis. She was placed on a biVAD and transplant list