Inflammatory Disorders

Updated Fall 2012 by Renee Redman From the notes of Nancy Jenkins

Overview of Today’s Lecture

A & P Review Endocarditis- infection of the endocardial surface

of the heart

Myocarditis- a focal or diffuse inflammation of the myocardium

Pericarditis- inflammation of the pericardial sac (the pericardium)

Anatomy and Physiology review

Anatomy and Physiology review

A- Aortic Valve

B- Mitral Valve

D- Tricuspid Valve

- Pulmonary Valve

Anatomy and Physiology Review

Blood enters the right atrium and moves through the _______ into the right ventricle.

Blood then moves from the right ventricle into the pulmonary artery via the _________.

A- Aortic Valve

B- Mitral Valve

C- Pulmonary Valve

D- Tricuspid Valve

Anatamy and Physiology Review (Cont’d)

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

Finally, it travels through the _____ and out of the heart.

A- Aortic Valve

B- Mitral Valve

C- Pulmonary Valve

D- Tricuspid Valve

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 –often bacterial Streptococcus viridans Staphylococcus aureus

Other Etiologies Viruses- Coxsackie B Fungi – Candida alibcans

Etiology and Pathophysiology

Occurs when blood turbulence within heart allows causative agent to infect previously damaged valves or other endothelial surfaces

Etiology and Pathophysiology

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

circulation – 50% of patients with IE will have systemic

embolization

Endocarditis

Infection of the innermost layers of the heart May occur in people with congenital and

valvular heart disease 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

Classifications of Endocarditis

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

Subacute Infective Endocarditis SBE– Gradual onset– Systemic manifestations

Prosthetic Valve Endocarditis Or named by cause (IVDA endocarditis, Fungal IE)

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- less common now (20% of cases)

Prior history of endocarditis Aging (50% associated with aortic stenosis) Invasive procedures- (introduce bacteria into blood stream)

(surgery, dental, etc) Permanent Central Venous Access- MRSA IV drug users Valve replacements Renal dialysis

Nursing Assessment

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

disease– Previous endocarditis – Staph or strep infection– Immunosuppressive therapy– Recent surgeries and procedures

Nursing Assessment

Functional health patterns– IV drug abuse– Alcohol abuse

Nursing Assessment

Nonspecific Clinical Manifestations– Weight changes– Chills– Low grade fever in 90% patients– Malaise

Nursing Assessment

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

Nursing Assessment

– Dyspnea on exertion – Night sweats – Chest, back, abdominal pain– Also consider s/s related to embolization to

specific organ – New or changing heart murmur

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- most have murmurs– 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

Clinical Manifestations

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

endocarditis Manifestations secondary to embolism

Heart Sounds Assessment Video

Auscultating Heart Sounds

The aortic area or right sternal border (RSB) is at the right 2nd intercostal space, just under and to the right of the angle of Louis (sternal angle)

The pulmonic area or left upper sternal border (LUSB) is at the left 2 nd intercostal space

The tricuspid area or left lower sternal border (LLSB) is at the left fifth intercostal space

The mitral area or apex is at the PMI -- the 5th intercostal space in midclavicular line

Past Medical History

Recent surgeries or procedures– Cardiac Cath,dental, urologocial, gynecological

(including vaginal or c-section deliveries)

Hx of IV drug use

Central line placement

Dialysis

Infections (recent UTI, URI or skin infection)

Immunosuppression

Diagnostic Tests

Blood Cultures- most likely positive unless recent antibiotic tx

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

serum creatinine,CXR, and EKG

Echocardiogram-

Major Diagnostic Criteria

Have at least two:– Positive blood culture– New or changed murmur– Echo positive for vegetation or mass

Could have:– CXR shows cardiomegaly– EKG with conduction A-V block

Diagnostic Criteria

Diagnostic Criteria

Medications

Antibiotics– IV for 4-8 weeks – Monitor peaks and troughs of certain drugs– Monitor BUN and Creatinine.– Evaluate effectiveness of treatment with repeated blood

cultures.– Unclear of success of oral antibiotics

Additional Treatment

Fungal infections- poor responsive to drug therapy

May require valve replacement Relapses are common Bedrest usually not indicated unless febrile,

HF or other complications

Nursing Diagnoses

Decreased cardiac output r/t valve insufficiency and altered rhythm

Activity intolerance r/t alternation in o2 transport system secondary to valve dysfunction

Hyperthermia r/t infection of endocardium Risk for Ineffective Tissue Perfusion-emboli Ineffective Health Maintenance

Complications

Emboli (50% incidence)– Right side- pulmonary emboli (esp. with IV drug abuse)– Left side-brain, spleen, heart, limbs, etc

CHF-check edema, rales, VS Arrhythmias- A-fib, conduction blocks Death

.

Treatment Goal

Return to baseline cardiac function ADL’s without fatigue Prevent recurrence

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 high risk patients – Removal or drainage of infected tissue– Renal dialysis– Ventriculoatrial shunts– Dental/oral manipulation, extraction or cleaning– Respiratory tract biopsy or incision– GI/GU- if infection present (ex, UTI or wound)

Video Review- Endocarditis

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.

Etiology/Pathophysiology

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

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

illness– Can result in 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

Multiple Causes of Myocarditis

Myocarditis- Assessment

Early s/s – Fever, fatigue – Malaise, mylagias– Dyspnea, lymphadenopathy– Nausea, vomiting

Myocarditis- Assessment

Cardiac s/s 7-10 days after viral infection– Pleuritic chest pain (pericardial friction rub)

Pericarditis frequently occurs with myocarditis- check friction rub

– Tachycardia– Arrhythmias- PVCs, PACs, Atrial Tachycardias,

Signs of heart failure –late cardiac s/s– S3 heart sound, crackles, JVD, syncope, edema

Myocarditis- Assessment

Sudden Death-– In young adults Myocarditis is the cause of up to

20% of sudden cardiac death

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

Biopsy Video

Myocarditis Treatment

Manage cardiac symptoms Viral – antibiotics for secondary 58% adults recover on own Treatment Goal

– Decrease workload of the heart so it can heal

Medications

Digoxin- use cautiously! – Improves CO but causes dysrhytmias in these patients

HF drugs- ACE, diuretics, beta blockers etc Immunosupressive therapy

– IVIG, prednisone, etc– Evidence inconclusive

Anticoagulants- – Reduces risks of thrombus in low EF

Other Treatments

Bedrest and activity restrictions- Why important??

**Activities may be limited for 6 months- 1 yr. O2 Intraaortic balloon pump Ventricular assist device Transplant

Nursing Diagnoses

Activity Intolerance Decreased CO Anxiety Excess fluid Volume

– watch for signs of heart failure; adventitious lung sounds; complications

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.

Pericardium Anatomy

Composed of two layers Visceral pericardium (inner) Parietal layer (outer) Pericardial space is inbetween

– Contain about 10-15ml of serous fluid– Provides lubrication– Decreases friction

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 mls before show

up on x-ray. Can have 1000 mls.

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-– 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

Pericardial Friction Rub

Hallmark finding of pericariditis High pitched rubbing, scratching, grating sound Best auscultated

– Left lower sternal border of chest– Patient leaning forward

May be intermittent Sound with pulse (not respirations…not pleural

effusion)

Pericardial Friction Rub

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

Diagnostic Tests- to R/O

EKG- 90% have ekg changes: serial ekg’s– ST elevation, PR changes, differ from MI

CBC- WBC, ESR and CRP Cardiac Enzymes-

– elevated but not as much as with MI

Echo- for wall movement CXR- may be normal CT or MRI- for pericardial effusion Pericardiocentesis fluid for analysis- attempt to determine

cause

ECG in Pericarditis

Medications

Antibiotics to treat bacterial pericarditis ASA or tylenol NSAIDS- ibuprofen Corticosteroids

– Typically reserved for patients with autoimmune conditions or not responding to NSAIDS

Pericarditis Video Review

Livestrong Pericarditis Video

Complications of Pericarditis

Pericardial Effusion- an accumulation of excess fluid in the pericardium

Cardiac Tamponade- as the pericardial effusion increases in volume it causes increased intrapericardial pressure resulting in compression of the heart

Pericardial Effusion

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

and tachypnea Phrenic nerve involvement- hiccups Laryngeal nerve- hoarseness Heart sounds distant and muffled

Pericardial Effusion- EKGElectrical Alternans

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

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

Pulsus Paradoxus

http://youtu.be/jTsjCZ9QxW8

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– Fluid removed from pericardium– Guided by EKG and echo– Complications: worsening cardiac tamponade, arrhythmias,

pneumothorax, myocardial laceration

Pericardiectomy– Complete or partial removal

Pericardial window– Surgical procedure to allow shunting

Sclerosing agent– Bonds layers together. Not common. Malignancy.

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– Loss of elasticity of pericardial sac

See signs of HF and cor pulmonale– DOE, fatigue, peripheral edema, wt loss…– Most relate to decreased cardiac output– Occurs over extended time (chronic)

Chronic Constrictive Pericarditis

Most prominent finding is jugular vein distention (JVD)

NO pulsus paradoxus Pericardial knock- early diasystolic sound

Treatment of choice pericardiectomy

Nursing Diagnoses for Pericarditis

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

Specific Nursing Assessment

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

Case Study

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 = 102º 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.

Case questions

1. Which of the following conditions constitutes the most likely diagnosis in this patient’s case?A. myocardial infarctionB. Dressler’s syndromeC. pericarditisD. hypertrophic subaortic stenosisE. cardiac tampanode

2. Which of the following methods represents the most appropriate next diagnostic step in working up this patient’s condition?A. angiographyB. CT scanC. technetium-99 perfusion scanD. magnetic resonance imagingE. echocardiography

3. Which of the following represents the most appropriate treatment in the management of this patient?A. non-steroidal inflammatory drugsB. cardiac catheterization with angioplastyC. coronary artery bypass graft procedureD. emergent IV administration of heparinE. pericardiocentesis