Transcript Inflammatory Disorders - Austin Community College

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
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Causative organism more virulent
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Streptococcus viridans
Staphylococcus aureus
Viruses
Fungi
Etiology and Pathophysiology
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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
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Endocarditis
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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
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Fibrin, leukocytes, platelets, and microbes
Adhere to the valve or endocardium
Embolization of portions of vegetation into circulation
Classifications of Endocarditis
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Acute Infective Endocarditis
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Subacute Infective Endocarditis SBE- most common
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Abrupt onset
Rapid course
Staph Aureus
Gradual onset
Systemic manifestations
Prosthetic Valve Endocarditis
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
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
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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-(HIV)
Recent surgeries and procedures
Nursing Assessment
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Functional health patterns
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IV drug abuse
Alcohol abuse
Weight changes
Chills
Nursing Assessment
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Diaphoresis
Fever
Bloody urine
Exercise intolerance
Generalized weakness
Fatigue
Cough
Nursing Assessment
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Dyspnea on exertion
Night sweats
Chest, back, abdominal pain
Collaborative Care
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Fungal and prosthetic valve endocarditis
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Responds poorly to antibiotics
Valve replacement is adjunct procedure
Assesment endocarditis
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Infection and emboli
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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
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Painful, pea-size, red or purple lesions
On finger tips or toes
Osler’s nodes
Roth spots
Roth’s Spots
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hemorrhagic retinal lesions
Diagnostic Tests
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Blood CulturesEchocardiogram-TEE best- see vegetations
Other- WBC with differential, CBC,ESR,
serum creatinine,CXR, and EKG
Echocardiogram-video
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Mitral Valve involvement
Echocardiogram-
Diagnostic Criteria
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Duke criteria
2 major
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Blood cultures and vegetations present
5 minor
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symptoms
Treatment- Medications
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Antibiotics
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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:
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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
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Risk for Imbalanced Body Temperature
Risk for Ineffective Tissue Perfusion-emboli
Ineffective Health Maintenance
Complications
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Emboli (50% incidence)
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CHF- 80% incidence with involvement of aortic valve
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Right side- pulmonary emboli (esp. with IV drug abuseWhy??)
Left side-brain, spleen, heart, limbs,etc
check edema, crackles, VS
Arrhythmias- A-fib
Death
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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
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Mitral valve prolapse without regurgitation
Coronary artery disease
People with pacemakers/ defibrillators
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• Prophylactic antibiotics are
generally recommended only
for people in the “High Risk”
category
Collaborative Care
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Prophylactic treatment for patients having
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Removal or drainage of infected tissue
Renal dialysis
Ventriculoatrial shunts
Dental, oral, or upper respiratory tract procedures
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Endocarditis video review
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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
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Myocarditis-video
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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 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
Assessment myocarditis
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Infection and CHF
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Fatigue,DOE
Tachycardia
Arrhythmias- PVCs, PACs, Atrial Tachycardias,
Chest pain
Signs of heart failure (S3, etc.)
Pericarditis frequently occurs with myocarditischeck friction rub
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 (EMB)
Medications
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Antibiotics
Antiviral with interferon-a
IVIG- experimental trials
Corticosteroids or immunosuppressents
HF drugs- ACE, diuretics, beta blockers etc
Antiarrhythmics
Anticoagulants- Why??
Other Treatments
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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
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Activity Intolerance
Decreased CO
Anxiety
Excess fluid Volume
Pericarditis
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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
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Pericarditis
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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
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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
Pericardial friction rubdiaphragm at LL sternal
border in knee chest
position
– Fever
– 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
Diagnostic Tests- to R/O
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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
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ASA or tylenol
NSAIDS- ibuprofen
Corticosteroids
Pericarditis video review
Livestrong Pericarditis Video
Complications of Pericarditis
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Pericardial Effusion- an accumulation of
excess fluid in the pericardium
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Cardiac Tamponade- an increase in
intracardial pressure caused by pericardial
effusion that results in compession of the
heart
Pericardial Effusion-video
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Can occur rapidly or slowly
Pulmonary compression-cough, dyspnea,
and tachypnea
Phrenic nerve involvement- hiccups
Laryngeal nerve- hoarseness
Pericardial Effusion- EKG
Electrical 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-
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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
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cardiac tamponade with aortic dissection
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PERICARDIUM
CARDIAC
TAMPONADE
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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
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-now use echo or fluoroscopy
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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)
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
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
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Acute Pain
Ineffective Breathing Pattern
Risk for Decreased Cardiac Output
Activity Intolerance
Review Specific Nursing Assessment for
Inflammatory Heart Disorders
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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?
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Significance of orthostatic hypotension, wide
pulse pressure and tachycardia?
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Decreased cardiac output, aortic insufficiency
Significance of abdominal tenderness,
hematuria, joint pain, and petechia?
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Indicates embolization.
Clinical Manifestations
in relation to J.F.
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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
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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?
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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
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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