Transcript Inflammatory Disorders - Austin Community College

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

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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


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Streptococcus viridans
Staphylococcus aureus
Other Etiologies

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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

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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
–
–
–

Subacute Infective Endocarditis SBE
–
–
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Abrupt onset
Rapid course
Staph Aureus
Gradual onset
Systemic manifestations
Prosthetic Valve Endocarditis
Or named by cause (IVDA endocarditis, Fungal IE)
Bacterial Endocarditis of the Mitral
Value
Fig. 37-2
Sequence of Events in Infective Endocarditis
Fig. 37-3
Risk Factors- endocarditis
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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
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Subjective Data
–
–
–
–
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History of valvular, congenital, or syphilitic cardiac
disease
Previous endocarditis
Staph or strep infection
Immunosuppressive therapy
Recent surgeries and procedures
Nursing Assessment
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Functional health patterns
–
–
IV drug abuse
Alcohol abuse
Nursing Assessment
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Nonspecific Clinical Manifestations
–
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–
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Weight changes
Chills
Low grade fever in 90% patients
Malaise
Nursing Assessment
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–
–
–
–
–
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Diaphoresis
Bloody urine
Exercise intolerance
Generalized weakness
Fatigue
Cough
Headache
Nursing Assessment
–
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–
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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
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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

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Painful, pea-size, red or purple lesions
On finger tips or toes
Osler’s nodes
Roth spots
Roth’s Spots
•
hemorrhagic retinal lesions
Clinical Manifestations
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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
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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
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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
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Have at least two:
–
–
–
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Positive blood culture
New or changed murmur
Echo positive for vegetation or mass
Could have:
–
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CXR shows cardiomegaly
EKG with conduction A-V block
Diagnostic Criteria
Diagnostic Criteria
Medications

Antibiotics
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–
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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
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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
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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
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Emboli (50% incidence)
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–
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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
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Return to baseline cardiac function
ADL’s without fatigue
Prevent recurrence
Prevention
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Eliminate risk factors
Patient teaching
Risk Stratisfication for IE
High Risk–
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Mechanical prosthetic heart valve
Natural prosthetic heart valve
Prior infective endocardititis
Valve repair with prosthetic material
Most congenital heart diseases
Moderate Risk–
–
–
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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
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Prophylactic treatment for high risk patients
–
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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
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Myocarditis
–
–
–
–
–
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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 cardiomyopathyheart 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
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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
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Early s/s
–
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Fever, fatigue
Malaise, mylagias
Dyspnea, lymphadenopathy
Nausea, vomiting
Myocarditis- Assessment
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Cardiac s/s 7-10 days after viral infection
–
Pleuritic chest pain (pericardial friction rub)
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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
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Sudden Death–
In young adults Myocarditis is the cause of up to
20% of sudden cardiac death
Diagnostic Tests
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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
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Manage cardiac symptoms
Viral – antibiotics for secondary
58% adults recover on own
Treatment Goal
–
Decrease workload of the heart so it can heal
Medications
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Digoxin- use cautiously!
–
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HF drugs- ACE, diuretics, beta blockers etc
Immunosupressive therapy
–
–
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Improves CO but causes dysrhytmias in these
patients
IVIG, prednisone, etc
Evidence inconclusive
Anticoagulants–
Reduces risks of thrombus in low EF
Other Treatments
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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
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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
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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
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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
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Inflammation and pain
–
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Pericardial friction rubFever
Substernal, sharp, pleuritic chest pain
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Inc. with coughing, breathing,turning,lying flat
Dec. with sitting up and leaning forward
Referred to trapezius muscle
Dyspnea
Pericardial Friction Rub
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Hallmark finding of pericariditis
High pitched rubbing, scratching, grating
sound
Best auscultated
–
–
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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
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EKG- 90% have ekg changes: serial ekg’s
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CBC- WBC, ESR and CRP
Cardiac Enzymes–
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ST elevation, PR changes, differ from MI
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
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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
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Livestrong Pericarditis Video
Complications of Pericarditis
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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
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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- EKG
Electrical 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
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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
PERICARDIUM
CARDIAC
TAMPONADE

Original heart size
Excess pericardial fluid
Cardiac tamponade
Definition- a decrease in
systolic BP with
inspirations that is
exaggerated in 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
Pulsus Paradoxus
http://youtu.be/jTsjCZ9QxW8
Determination of Pulsus Paradoxus
1. Place the patient in a position of comfort and take their systolic blood
pressure during baseline respiration.
2. Raise sphygmomanometer pressure until Korotkoff sounds disappear.
3. Lower pressure slowly until first Korotkoff sounds are heard during
early expiration with their disappearance during inspiration
4. Record this pressure.
5. Very slowly lower pressure (1mm at a time) until Korotkoff sounds are
heard throughout the respiratory cycle with even intensity.
6. Record this pressure.
7. The difference between the two recorded pressures is the Pulsus
Paradox.
8. 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
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Pericardiocentesis
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Pericardiectomy
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Complete or partial removal
Pericardial window
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Fluid removed from pericardium
Guided by EKG and echo
Complications: worsening cardiac tamponade, arrhythmias,
pneumothorax, myocardial laceration
Surgical procedure to allow shunting
Sclerosing agent
–
Bonds layers together. Not common. Malignancy.
Pericardial
Window
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.
Cardiac Tamponade and
treatment
Chronic Constrictive Pericarditis
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Starts with acute then scarring and fibrosis
occur
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Loss of elasticity of pericardial sac
See signs of HF and cor pulmonale
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–
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DOE, fatigue, peripheral edema, wt loss…
Most relate to decreased cardiac output
Occurs over extended time (chronic)
Chronic Constrictive Pericarditis
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Most prominent finding is jugular vein
distention (JVD)
NO pulsus paradoxus
Pericardial knock- early diasystolic sound

Treatment of choice pericardiectomy
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Nursing Diagnoses for Pericarditis
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Acute Pain
Ineffective Breathing Pattern
Risk for Decreased Cardiac Output
Activity Intolerance
Specific Nursing Assessment
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Paradoxical pulse
Murmur
Pericardial friction rub
Emboli
Chest pain
CHF
Comfort Measures
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O2
Bedrest
Positioning
Prevent complications of immobility
Psychological support
Review- animations
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Endocarditis
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Myocarditis
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Pericarditis
Case Study- Endocarditis
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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 18month 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
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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
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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.
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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 infarction
B. Dressler’s syndrome
C. pericarditis
D. hypertrophic subaortic stenosis
E. cardiac tampanode
2. Which of the following methods represents the most appropriate next diagnostic step in
working up this patient’s 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