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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