Traumatic, Infectious, & Inflammatory Heart Conditions PDF

Traumatic, infectious, and inflammatory heart conditions. Fiona Peterman, PA-C Assistant Professor Chamberlain University  Course outcomes CO1: Analyze cardiovascular anatomy structures and physiology CO2: Develop a differential diagnosis, based on criti...

Traumatic, infectious, and inflammatory heart conditions. Fiona Peterman, PA-C Assistant Professor Chamberlain University  Course outcomes CO1: Analyze cardiovascular anatomy structures and physiology CO2: Develop a differential diagnosis, based on critical evaluation of history, patient signs/symptoms, physical exam and lab findings for patients with cardiovascular conditions. CO3: Select appropriate diagnostic tests and lab studies for patients with cardiovascular conditions. CO4: Formulate an appropriate, comprehensive, treatment plan for patients with cardiovascular conditions. CO5: Integrate health promotion and prevention strategies for patients with cardiovascular conditions to promote wellness.  Learning objectives Overview to various cardiology topics Definition of terms Epidemiology and etiology of disease Prevalence of disease Risk factors History & physical exam Clinical findings Diagnosis/work up Management and other considerations DDx  Topics Endocarditis Pericardial Disorders Pericarditis Constrictive pericarditis Pericardial effusion Cardiac tamponade Myocarditis Endocarditis  Endocarditis Definition Infective endocarditis (IE) is caused by infection or inflammation of the inner lining of the heart (endocardium), most commonly affecting the heart valves. Noninfective endocarditis (NIE) results from the formation of sterile platelet and fibrin thrombi on cardiac valves and endocardium. Endocarditis  Epidemiology of Endocarditis Infective endocarditis: Most common form of endocarditis Incidence: 11–15 cases per 100,000 persons per year Mean age: 60.8 years (> 50% are > 50 years of age) 3 times more common in men Noninfective endocarditis: Rare Often found on autopsy Incidence: 0.9%–1.6% Common age group: 30–70 years No gender predilection  Infective Endocarditis Infective endocarditis may be caused by numerous organisms including: Staphylococci: Staphylococcus aureus (most common), S. epidermidis Streptococci: Streptococcus viridans (commonly after dental procedures), S. pneumoniae, S. bovis (associated with colon cancer) HACEK group: Haemophilus, Actinobacillus (now known as Aggregatibacter), Cardiobacterium, Eikenella, Kingella Other bacterial causes: Enterococcus, Coxellia burnetiid, Brucella, Bartonella Fungi: Candida albicans, Aspergillus  Noninfective Endocarditis Libman-Sacks endocarditis: Rheumatic endocarditis: Due to circulating immune Due to antigen-antibody reaction after group complexes A Streptococcus pharyngitis Associated with: Affects mitral > aortic valve Systemic lupus erythematosus Löffler endocarditis: Affects mitral valves > aortic Associated with hypereosinophilic syndrome valves Due to eosinophilic infiltration and Thrombotic (marantic) endocarditis: tissue damage Malignancy (due to Iatrogenic trauma to the cardiac valves metastases seeding the heart valves) Other autoimmune conditions Hypercoagulable states (rare): Rheumatoid arthritis Chronic infections (e.g., tuberculos Systemic scleroderma is) Vasculitis  Risk factors and Pathophysiology (Non-infective endocarditis) Noninfective endocarditis Endothelial injury to the valve leaflets due to: Trauma Circulating immune complexes Cytokines Antigen-antibody reactions Platelet activation and deposition occurs (often during a hypercoagulable state). Thrombus is interwoven with: Fibrin Immune complexes Vegetations are easily dislodged → embolic complications  Risk factors (Infective endocarditis) The following are risk factors for IE: Heart disease: Rheumatic heart disease Valvular abnormalities Congenital defects Presence of a prosthetic valve Age > 60 years IV drug use/parenteral entry (most commonly affects the tricuspid valve) Poor dentition Implanted devices or catheters Immunosuppression Previous history of endocarditis  Risk factors and Pathophysiology (Infective endocarditis) Infective endocarditis Predisposing factors: Endocardial abnormality or injury Bacteremia Damaged endothelium → platelet and fibrin deposition → adherence by microorganisms Proliferation and invasion by organisms → inflammation → vegetation development → valve destruction Release of septic emboli → embolic complications and/or metastatic infection  Test yourself What is the main component of non-bacterial thrombotic endocarditis? A. Fibrin and platelet B. Red blood cells and myocytes C. White blood cells and bacteria D. LDL cholesterol  Classification (By Clinical course) Acute infectious Subacute infectious endocarditis: endocarditis: More gradual More sudden onset of onset of symptoms symptoms Progresses more slowly Progresses more rapidly (weeks to months) Larger vegetations Smaller vegetations More commonly affects More commonly affects normal valves Fatal if not treated congenitally abnormal or promptly diseased valves Most common cause is S. Patients may survive for aureus. months untreated. Most common cause is S. viridans.  Classification (By Valve type) Native valve endocarditis: Prosthetic Accounts for 78% of cases valve endocarditis: Further subdivided into: Further subdivided into: Early: Community acquired < 60 days after valve placement (most common) Often from contamination during Healthcare associated surgery Beware of antimicrobial-resistant IV drug use organisms. Intermediate: 60–365 days after Most often associated valve placement with: Late: > 1 year after valve placement Staphylococcus Usually involves similar Streptococcus organisms to native valve endocarditis HACEK organisms Associated with a higher risk of complications and mortality  Classification (By Location) Left-sided endocarditis: Right-sided Mitral valve endocarditis (most Aortic valve common in IV drug use): Tricuspid valve Pulmonic valve  Clinical Presentation Presentation and course depend on the etiology, location of vegetations, and severity. General signs and symptoms: The following are more frequently seen in IE than NIE: Fever (endocarditis should be suspected in a patient with a fever of unknown origin) Night sweats Fatigue Loss of appetite Weight loss Myalgias and arthralgias  Clinical Presentation Cardiac findings/physical examination New or changed cardiac murmur: Mitral regurgitation Tricuspid regurgitation Aortic regurgitation Tachycardia Arrhythmia: Potentially due to spread of the infection and myocardial abscess formation. Results in disruption of the atrioventricular conduction system → conduction delay or heart block.  Clinical presentation (Extracardiac findings) Splinter hemorrhages: Small areas of red discoloration under the nails. Due to microemboli in capillaries. Splinter Hemorrhage Causes, Treatment (health.co m)  Clinical presentation (Extracardiac findings) Osler nodes: Painful red nodules on Osler node on the 4th digit of the pads of the fingers and left hand toes Due to immune complex deposition and inflammation Osler's node on the fourth digit of the left hand. | D ownload Scientific Diagram (researchgate.net)  Clinical presentation (Extracardiac findings) Janeway lesions: Small, painless, erythematous lesions on the palms or soles Due to septic emboli and microabscesses Janeway lesion showing as painless, macular, hemorrhagic, irregularly shaped lesions on patient's palm  Clinical presentation (Extracardiac findings) Roth spots: Red spots with pale centers on fundoscopic exam Due to retinal hemorrhages Petechiae Conjunctiva hemorrhage Roth Spots in Native Valve Endocarditis (degruyt com)  Test yourself How do you describe splinter hemorrhages seen on infective endocarditis? A. Small hemorrhages seen in the retina B. Painful erythematous swelling in the skin and subcutaneous tissues of hands C. Microthrombi in the nailbed D. It is popularly known as Janeway lesions  Mnemonic Signs of IE can be remembered with the mnemonic "FROM JANE": Fever Roth spots Osler nodes Murmur Janeway lesions Anemia Nail bed hemorrhage (splinter hemorrhages) Emboli  Complications from endocarditis Cardiac: Perivalvular abscess Valve insufficiency Valve rupture Heart failure Pericarditis → cardiac tamponade Renal: Glomerulonephritis Antibiotic-induced nephrotoxicity Metastatic infections: Splenic abscess Mycotic aneurysm → cerebral hemorrhage Brain abscess or meningitis Septic arthritis Osteomyelitis Renal abscess Pneumonia or lung abscess Death: mortality rate up to 40%  Diagnosis Overview Based on several different factors: Echocardiogram Labs Blood cultures ECG Modified Duke Criteria  Diagnosis Transthoracic echo (TTE): Findings: Used as an Valvular vegetations: initial screening tool Size A negative study does not Mobility exclude the diagnosis. Calcifications Transesophageal echo (TEE): Complications: More sensitive, but more Valvular insufficiency invasive Abscess Should be performed if TTE is Cannot determine the negative and suspicion for endocarditis is high cause of vegetations (IE versus NIE) Depiction of transesophageal ECG. Patients are generally sedated for this procedure. The echo transducer is lowered into the esophagus, which places it Transesophageal echocardiography images demonstrating vegetations on the mitral valve in a patient with non-infective endocarditis due to malignancy. The solid arrow is pointing to a vegetation on the anterior leaflet, and the dotted arrow is Transesophageal echocardiography image showing 2 vegetations (red arrows) on the mitral valve in a patient with endocarditis  Supporting w/u – Lab findings The following are nonspecific but may signal IE: Blood cultures: 3 sets should be obtained from different sites. Must be obtained prior to starting antibiotics. Negative cultures do not rule out IE. Serology: Consider pursuing if cultures are negative Useful for fastidious organisms CBC: Leukocytosis Normocytic anemia Inflammatory markers: ↑ Erythrocyte sedimentation rate ↑ CRP  Supporting w/u – Lab findings The following may be useful in NIE: Antinuclear antibodies Lupus anticoagulant Antiphospholipid antibodies  Supporting w/u – Imaging studies ECG: Generally normal unless there is extension of the infection A baseline tracing should be performed in all patients. Possible findings: Heart block or atrioventricular dissociation Bundle branch block Chest X-ray: Can rule out other causes of symptoms Potential findings in endocarditis: Septic emboli to the lungs Pulmonary edema and cardiomegaly CT: Can be used to assess for sites of metastatic infection May be useful if an underlying malignancy is suspected (for NIE) MRI: performed if cerebral embolic events are suspected  Duke Diagnostic criteria The Duke diagnostic criteria is a set of clinical criteria that can aid in the diagnosis of IE. Must meet 1 of the following for a definitive diagnosis of IE: 2 major criteria 1 major plus 3 minor criteria 5 minor criteria  Duke Diagnostic criteria Major criteria: Positive blood cultures (1 of the following): Typical organism for IE in 2 separate blood cultures Persistently positive cultures Single positive culture for Coxiella burnetii Findings of endocardial involvement (1 of the following): Positive echocardiogram: presence of vegetation, abscess, or new partial dehiscence of a prosthetic valve; must be performed rapidly if IE is suspected New valvular regurgitation  Duke Diagnostic criteria Minor criteria: Fever > 38°C (100.4°F) Risk factors/predisposing conditions: IV drug use, Predisposing heart condition, abnormal valves, etc. Vascular findings: Major arterial emboli Janeway lesions Conjunctival hemorrhages Septic infarcts Mycotic aneurysm Immunologic findings: Osler nodes Roth spots Glomerulonephritis Microbiologic findings by culture that do not meet major criteria Blood cultures that did not meet major criteria Echo that did not meet criteria for major  Test yourself Which of the following is NOT a major criteria based on the Duke criteria for endocarditis? A. Single positive blood culture for Staphylococcus aureus B. Persistently positive blood cultures C. Vegetations or new murmur seen on echocardiography D. Single positive blood culture for coxiella burnetti Medical management Starting Empiric Antibiotics (Admission, inpatient) Recommended consultations: Infectious disease Cardiology Cardiothoracic surgery  Medical management (Infectious Endocarditis) Prompt initiation of IV antibiotics is necessary if the patient is acutely ill Initiate empiric antibiotics: Native valve: Vancomycin+ Gentamycin/ or Ceftriaxone Nafcillin + Gentamycin Prosthetic valve: Vancomycin+ Gentamicin + Rifampin Fungal Infection: Amphorectin B (treat 6-8 weeks) Tailor antibiotics or antifungals based on: Identified pathogen Sensitivities Duration of therapy: 4-6 weeks  Medical management (Infectious Endocarditis) Repeat blood cultures every 24 hours until negative. Serial PEs should be done to make sure no complications arise Patients might have fever up to a week after starting Antibiotics Once hemodynamically stable, negative blood culture, and surgery was consulted: Can discuss doing outpatient parenteral/ IV therapy Need to be fully capable, have full assess to medical care incase of complications Have to monitor with weekly labs  Medical management (Non-Infectious Endocarditis) Medical management of NIE Treatment for the underlying disorder Anticoagulation (unfractionated or low-molecular-weight heparin)  Surgical management Valve repair or replacement is indicated for: Heart failure Persistent/refractory infection Embolic events Prosthetic valve dehiscence Perivalvular abscess Conduction abnormalities Fungal infection Implanted hardware removal (e.g., pacemaker) is indicated if: Definite lead or hardware infection Sepsis Pocket infection Persistent bacteremia Staphylococcus bacteremia Intraoperative vegetation findings on the aortic valve in a patient with endocarditis  Endocarditis Prophylaxis Indications Pre-procedure antibiotics: High-risk Antibiotic options: procedures: Dental procedures involving cleaning, Amoxicillin (preferred manipulation of the gingiva or mucosa with patients with h/o of infective ) endocarditis. 2g 30-60 min before Respiratory tract procedures involving biopsy or manipulation of mucosa procedure Procedures involving infected skin/ MSK tissues Cephalexin Including abscess I&D Clindamycin (if PCN Prophylaxis indicated for: Prosthetic (artificial) valves allergy) Unrepaired cyanotic congenital heart disease Repaired congenital heart defect with prosthetic material Prior episode of endocarditis Transplanted heart with valvulopathy  Endocarditis Prevention Anyone cured of IE are at higher risk for IE Antibiotic prophylaxis Dental hygiene: routine care! IV drug users: should be offered and enrolled in addiction treatment programs and counselling.  Test yourself Which of the following is NOT a risk factor for infective endocarditis (IE)? A. Dental/surgical procedure B. Intravenous drug abuse C. Intranasal drug abuse D. Active infection Pericarditis Pericarditis  Definition and classification Definition Pericarditis is an inflammation of the pericardium, the double-layered sac surrounding the heart. Clinical classification is based on duration. Acute (< 6 weeks) Fibrinous Effusive (serous or serosanguinous) Subacute (6 weeks to 6 months) Effusive-constrictive Constrictive Chronic (> 6 months) Constrictive Adhesive (non-constrictive)  Epidemiology Reported in 0.1%–0.2% of hospitalized patients Found in 5% of patients admitted to the emergency department (ED) for nonischemic chest pain Pericarditis is more common in men and those younger than 50 years of age.  Etiology Idiopathic (most common) After exclusion of other causes Viral infection Coxsackievirus B Influenza HIV Echovirus Bacterial infection Tuberculosis (most common cause worldwide) Streptococcus species (rheumatic fever) Lyme disease Pseudomonas Staphylococcus species Mycoplasma Fungal infection (very rare) Histoplasma Blastomyces Coccidioides Aspergillus Autoimmune disease Systemic lupus erythematosus Rheumatoid arthritis Sarcoidosis  Etiology Metabolic Uremia Hypothyroidism Cardiovascular Dressler syndrome Myocardial infarction Cardiac injury (e.g., following operation) Aortic dissection Chronic heart failure Cancer Lung cancer Breast cancer Leukemia Lymphoma Radiation therapy Drugs Procainamide Hydralazine Penicillin Isoniazid Chemotherapy  Definitions 1.Pleuritic pain: pain that is exacerbated with inspiration or exhalation and reduced or eliminated by holding respirations 2.Pericardial friction rub: a rasping, scratching, or grating sound with up to 3 components per cardiac cycle and best heard during expiration with the patient leaning forward. Associated with the rubbing of the 2 layers of the pericardium. 3.Pericardial knock: an early third heart sound 4.Kussmaul’s sign: absence of normal decline in jugular venous pressure with inspiration; also seen in tricuspid stenosis, right ventricular infarction, and restrictive cardiomyopathy 5.Paradoxical pulse: a drop by > 10 mmHg in systolic blood pressure (SBP) during inspiration (i.e., difference between the first SBP sound heard during exhalation and the first SBP sound heard audible throughout the respiratory cycle > 10 mm Hg)  Definitions 6. Electrical alternans: alternating QRS amplitudes. 7. Tamponade: pericardial effusion, usually of rapid onset, exceeding ventricular filling pressures and causing collapse of the heart with a markedly reduced cardiac output  Clinical presentation of pericarditis (Pain) Acute sx Chronic sx Severe/sharp Less severe Frequently: pleuritic May be absent if Sometimes: steady (may developing slowly get confused with acute myocardial infarction [MI]) Radiation: neck, shoulder(s), arm(s), trapezius  Etiology – Specific features Viral or acute idiopathic pericarditis: Chest pain 1–2 weeks after a viral-like illness is suggestive. Must exclude acute MI, postcardiac injury, drugs, etc. Most frequent complication is relapsing pericarditis. Postcardiac injury acute pericarditis: 1–4 weeks after a cardiac operation or blunt/penetrating trauma. Tuberculous pericarditis: Common cause of chronic pericardial effusion in developing countries In a patient with tuberculosis: positive fluid culture or pericardial biopsy revealing caseating granuloma confirms the diagnosis. Uremic pericarditis: Seen with severe renal failure or in patients on chronic dialysis.  Clinical presentation of pericarditis (Other symptoms) Acute sx Pain intensifies with lying supine& with coughing Pain improves with leaning forward Chronic sx May have dyspnea (SOB)  Clinical presentation of pericarditis (Physical examination) Acute sx May have neck vein distension Pericardial friction rub Chronic sx May have neck vein distension X-ray: Large cardiac silhouette  Pericarditis: Diagnostics EKG/ECG: Acute sx: Diffuse ST-segment elevation with upward concavity and without T-wave inversions. PR depressions Chronic sx: Electrical alternans with a large effusion. (Echocardiography/Echo) Isolated pericarditis: normal Acute sx: Pleural effusion Chronic sx: Pleural effusion Blood work: nonspecific (leukocytosis, ↑ESR, ↑CRP) ECG showing diffuse ST segment elevation and the absence of reciprocal ST segment depression  Pericarditis Complications Cardiac tamponade Pericardial effusion Constrictive pericarditis  Management Viral or idiopathic pericarditis Oxygen and analgesia Can be treated on outpatient basis with: Nonsteroidal anti- inflammatory drugs (NSAIDs) or high dose aspirin x7-14 days (e.g., ibuprofen, indomethacin) plus gastric protection Start to taper NSAID dose slowly after symptoms start to improve Adjuvant therapy with colchicine enhances response and reduces the recurrence rate Colchicine should be administered for a total of three months for patients with an initial episode of acute pericarditis. Short-term glucocorticoids can be used if NSAIDs/colchicine are ineffective or contraindicated If no improvement in 48 hrs  Management Who gets admitted? Fever Complications: signs of tamponade or large pericardial effusion Immunosuppressed patient Acute trauma Elevated cardiac troponin levels Specific treatments Initiation or intensification of dialysis in addition to NSAIDs in uremic pericarditis Antibiotics if an underlying infection is found Antituberculous therapy ± pericardiectomy  Constrictive Pericarditis Constrictive pericarditis is characterized by a thickened and scarred pericardial sac that lies around the heart and prevents proper diastolic filling. From chronic pericarditis & inflammation Restrictive ventricular filling  increase venous pressures, decrease stroke volume( decreased cardiac output)  Constrictive Pericarditis: Clinical Manifestations Symptoms: Signs: Dyspnea (MC symptom) Right sided HF signs: Fatigue, weakness Increased JVD, peripheral edema, Orthopnea Kussmaul’s sign Pericardial knock: Freq cough High pitched 3rd heart sound Weight gain Hepatomegaly, ascites Constrictive Pericarditis: Diagnostics CXR: pericardial calcification, clear lung fields. Normal to slightly increased heart size Echocardiography: pericardial thickening. EKG: Low-voltage QRS Atrial fibrillation in ⅓ of cases Constrictive Pericarditis: Treatment Complete pericardial resection (pericardiectomy) is the only definitive treatment and is best performed as early as possible Diuretics to reduce symptoms leading to surgery  Pericardiectomy Successful Radical Pericardiectomy for Porcelain Co nstrictive Pericarditis | JACC: Case Reports  DDx MI Aortic stenosis Stable/unstable angina Esophagitis Pneumonia TB Pneumothorax  Test yourself Which of the following is MOST likely to be expected in a patient presenting with viral pericarditis? A. The patient is more comfortable lying flat. B. The patient will not have a pulsus paradoxus. C. The patient will have elevated blood pressure D. The patient is most comfortable sitting upright and forward. Pericardial Effusion & Cardiac Tamponade Pericardial effusion  Definitions Pericardial effusion is the accumulation of fluid in the pericardial space. Can be secondary to pericarditis, uremia, cardiac trauma Cardiac tamponade is due to the rapid accumulation of pericardial fluid/pericardial effusion sufficient to impair cardiac filling and cause hemodynamic compromise The rate of fluid accumulation, and not necessarily the amount, is most important.  Epidemiology Pericardial effusion: The incidence is unknown. Has been observed in approximately 3% of autopsy subjects in studies Age: Can occur in all age groups Mean: 50–60 years Cardiac tamponade: Incidence: 2 cases per 10,000 people in the United States Occurs in approximately 2% of penetrating injuries More common in boys and men  Etiology – Infection Viral (most common): Bacterial: Coxsackievirus group B Staphylococcus aureus Streptococcus Influenza Neisseria Echovirus Legionella HIV Treponema pallidum EBV Mycobacterium tuberculosis CMV Parvovirus B19 Fungal: Varicella Candida Histoplasmosis Coccidioidomycosis  Other Etiologies Malignancy: Primary cardiac tumors Metastatic disease Trauma Penetrating chest trauma Post cardiac resuscitation Post-procedural occurrence: Cardiac surgery (postpericardiotomy syndrome) Radiation  Etiology – Autoimmune/connective tissue dz Autoimmune and connective tissue disease: Systemic lupus erythematosus Rheumatoid arthritis Ankylosing spondylitis Scleroderma Sarcoidosis Sjögren syndrome Vasculitis  Etiology – Other Other medical conditions: Post-myocardial infarction (Dressler syndrome) Heart failure Aortic dissection Uremia (chronic renal failure) Myxedema Amyloidosis Can be induced by drugs: Procainamide Hydralazine Isoniazid Minoxidil Phenytoin Anticoagulants Idiopathic  Pathophysiology Normal physiology of the heart: The pericardial space normally contains a small volume of serous fluid. Under normal circumstances, the pericardial fluid: Cushions the heart Provides a low-friction environment Allows the heart to move easily  Pathophysiology Pericardial effusion and cardiac tamponade: The pericardium has limited elasticity. Accumulation of pericardial fluid → ↑ pressure in the pericardial sac As pericardial effusion continues to increase → ↑ compression of the heart: ↓ Diastolic filling → venous congestion ↓ Stroke volume ↓ Cardiac output → hypotension and obstructive (cardiogenic) shock ↑ HR to maintain cardiac output as a compensatory mechanism The rate of fluid accumulation is important: If fluid were to fill the pericardial space rapidly (e.g., chest trauma), as little as 150 mL could lead to tamponade. If fluid accumulates slowly, the pericardial sac can stretch to accommodate approximately 2 L of fluid.  Pericardial effusion clinical presentation Symptoms: Without cardiac tamponade: Usually, no symptoms specific to effusion Symptoms may be related to the underlying condition (e.g., infection, uremia, autoimmune disease). With cardiac tamponade: Dyspnea Cough Chest pain (pericarditis): Worse when lying flat Improves when sitting up Lightheadedness Syncope Palpitations Hoarseness Fatigue  Physical exam The following may be seen with large pericardial effusions and cardiac tamponade: Vital signs: Hypotension, Tachycardia Cardiovascular: Pericardial friction rub (pericarditis) Muffled heart sounds Jugular venous distension Hepatojugular reflux Weakened peripheral pulses Pulsus paradoxus: a drop in systolic blood pressure of > 10 mm Hg during inspiration Respiratory: Dullness to percussion beneath the angle of the left scapula and egophony Diminished breath sounds (if pleural effusion is present) Peripheral: Edema and cyanosis  Physical exam Beck’s Triad The triad describes the classic findings in cardiac tamponade: Hypotension Jugular venous distension Muffled heart sounds on auscultation  Diagnosis ECG/EKG: Sinus tachycardia Low voltage of QRS complexes Diffuse ST elevation with PR depression (pericarditis) Electrical alternans: Consecutive QRS complexes that alternate in height Seen in large pericardial effusion or cardiac tamponade Electrical alternans on an ECG in a patient with a large pericardial effusion: The arrows point to the alternating amplitude of the QRS complex.  Diagnosis Chest X-ray: Might appear normal in conditions with low fluid accumulation Enlargement of the cardiac silhouette: Occurs when > 250 mL of fluid has accumulated Takes on a “water bottle” shape Lung fields are typically clear. Cardiomegaly due to pericardial effusion before and after drainage: (a) Chest X-ray demonstrating cardiomegaly due to the accumulation of pericardial effusion (b) There is resolution of this cardiomegaly after drainage of the fluid.  Diagnosis Transesophageal echocardiogram (TEE): Diagnostic test of choice High sensitivity and specificity Provides hemodynamic information Pericardial effusion appears as an echolucent space in the pericardial sac. Cardiac tamponade findings: Right atrial free-wall collapse during systole Right ventricle collapse during diastole Inferior vena cava dilation Echocardiogram showing pericardial effusion (echolucent region around the heart) A CT scan demonstrating pericardial effusion, measuring 19.27 mm  Diagnosis Pericardial fluid analysis and pericardial biopsy Pericardial fluid analysis and pericardial biopsy may be performed to determine the cause of the pericardial effusion. The following tests may be conducted on the pericardial fluid: Gram stain and cultures (including fungal) Cell count with differential Cytology Acid-fast bacillus stain and culture Viral PCR panel  Diagnosis Laboratory evaluation The following tests may be performed to ascertain the etiology of a pericardial effusion: CBC with differential BUN and creatinine Erythrocyte sedimentation rate and CRP Troponin Thyroid-stimulating hormone (TSH) Rheumatoid factor levels ANA Complement levels Quantiferon-TB assay HIV serology Management – Pericardial effusion Management of pericardial effusion Depends on the patient's stability and the underlying cause of effusion Identify and treat the underlying conditions. Medical therapy for inflammatory effusions or associated pericarditis: NSAIDs Colchicine Small effusions in a stable patient are usually self resolving → no need for any intervention Pericardial drainage (Pericardiocentesis) can be considered in: Large symptomatic effusions Uncertain etiology Management – Cardiac Tamponade Management of cardiac tamponade General considerations: Administer oxygen. Measures to ↑ cardiac output: IV fluid resuscitation Inotropic support (e.g., dobutamine) Pericardiocentesis: A needle is inserted into the pericardial space. Fluid is removed to relieve pressure on the heart. A catheter can be placed for periodic drainage. Subxiphoid approach for pericardiocentesis: This approach allows the drainage of pericardial fluid.  Management Surgical management: Allows for pericardial biopsy Preferred in traumatic pericardial effusions Options: Pericardiotomy Pericardial window (Surgical construction of an opening or window in the pericardium. It is often called subxiphoid pericardial window technique).  Test yourself Which of the following is a component of Beck’s triad? A. Hypertension B. Distended neck veins C. Lower leg edema D. Congestive heart failure  Acute Pericarditis Pericardial Cardiac Constrictive Effusion Tamponade Pericarditis Definition Inflammation of the ↑ Fluid in pericardial Pericardial effusion  Fibrotic calcified pericardium space pressure on the heart pericardium that limits limits ventricular ventricular diastolic diastolic filling and ↓ filling cardiac output Etiologies 2 MC: Idiopathic & Viral Same as acute Same as acute Same as (coxsackievirus & pericarditis pericarditis pericarditis echoviruses) may be traumatic Chronic Neoplastic, Autoimmune, inflammation inflammatory, etc. Dressler’s syndrome (post MI) Clinical 5 Ps of pericarditis: Distant (muffled) Becks Triad: Dyspnea Manifestatio Chest Pain heart sounds Hypotension R sided HF sx Pleuritic (CP) +/- sx of pericarditis ↑ JVP (peripheral edema, ↑ n Postural (CP) Distant heart JVP, hepatic Persistent (CP) sounds (effusion) congestion) Pericardial Friction Rub Pulsus paradoxus Pericardial knock Kussmaul's sign Pulsus paradoxus Kussmaul’s sign Diagnosis ECG: Diffuse ST elevations in ECG: Diffuse ST ECG: Electrical Echo: pericardial precordial leads with PR elevations in alternans, Low voltage thickening & depressions in same leads precordial leads with QRS complex calcification Echo: normal (maybe effusion) PR depressions in Used to r/o tamponade same leads Echo: ↑pericardial Echo:↑pericardial fluid fluid + diastolic - No hemodynamic collapse of cardiac compromise chambers  Myocarditis  Myocarditis Definition Myocarditis is an inflammatory disease of the myocardium. Epidemiology Incidence: approximately 10–22 cases per 100,000 people About 1%–5% of viral infections involve the myocardium. Affects more men than women More common in young adults Myocarditis  Etiology of Myocarditis Idiopathic (50% of cases) Genetic predisposition: Infectious organisms: Genetic defects in the Viral (most common in North America and structural proteins of myocytes Europe) ↑ Susceptibility to myocyte damage Bacterial Protozoal (most common in Africa, Asia, and Environmental causes: South America) Exposure to carbon monoxide Fungal Heavy-metal toxicity Immune-mediated disorders: Rheumatic fever Black widow venom Allergic reactions Drugs: Transplant rejection Doxorubicin Kawasaki disease Cyclophosphamide Sarcoidosis Systemic lupus erythematosus Cocaine Scleroderma Amphetamines Juvenile idiopathic arthritis Ethanol Vasculitis  Causes of Infectious Myocarditis Viral Bacterial Parasitic Fungal Coxsackie B virus Borrelia burgdorferi Trypanosoma cruzi Aspergillus Adenovirus Mycoplasma pneumoni Toxoplasma gondii Candida Parvovirus B19 ae Entamoeba histolytica Actinomyces Human herpesvirus 6 Mycobacterium tubercu Leishmania Blastomyces Epstein-Barr virus losis Coccidioides Cytomegalovirus Corynebacterium dipht Histoplasma Hepatitis C heriae Cryptococcus Influenza Staphylococcus Mucormyocises Poliovirus Neisseria gonorrhoeae Nocardia HIV Streptococcus Brucella Haemophilus influenzae Treponema pallidum Coxiella burnetti Rickettsia rickettsii  Pathophysiology Inflammation due to various etiologies leads to enlargement of the heart and dilation of all chambers. Causes of myocyte injury: Viral: direct viral toxicity, lymphocytic infiltration, and cytokines Bacterial: direct invasion or bacterial toxins Autoimmune: autoantibodies to myocyte components Toxins: hypersensitivity or direct effects Myocardial inflammation and injury → myocardial necrosis Severe and prolonged damage → fibrosis → chamber remodeling → dilated cardiomyopathy Consequences: Heart failure Cardiac arrhythmia Extension to the pericardium → pericarditis  Clinical presentation The clinical presentation can vary based on the severity and progression of symptoms. Most signs and symptoms are related to heart failure. Classification Myocarditis is classified based on temporal progression. Subclinical: absent or minimal symptoms Acute: heart failure develops in < 3 months. Chronic: heart failure develops in > 3 months. Symptoms Fever Chest pain Dyspnea Orthopnea Loss of appetite Abdominal pain Fatigue Decreased exercise tolerance  Physical exam findings Tachycardia Arrhythmia Peripheral edema Hepatomegaly Pulmonary rales Jugular venous distention Murmur → may indicate chamber enlargement: Mitral regurgitation Tricuspid regurgitation S3 and S4 gallops Pericardial friction rub (pericarditis)  Complications from myocarditis Cardiogenic shock Myocardial infarction Dilated cardiomyopathy Cardiac arrhythmias Mural thrombus with systemic emboli Sudden cardiac arrest  Diagnosis Laboratory studies: Chest X-ray: ↑ Erythrocyte sedimentation rate Normal to enlarged heart (ESR) Cardiomegaly ↑ CRP Indications of heart failure: ↑ Troponin Pulmonary venous congestion ↑ Natriuretic peptide Pleural effusion Viral testing may aid in identifying Cardiac imaging the causative agent. Rheumatological screening for Echocardiogram: autoimmune causes Should be performed in all patients ECG: with suspected myocarditis May be normal in early or mild disease ST changes: Possible findings: Often nonspecific Left ventricular dilation Diffuse ST elevation signals seen Ventricular systolic dysfunction in pericarditis Arrhythmia Mitral or tricuspid regurgitation Pericardial effusion Conduction delays Intracardiac thrombi Excludes other causes of heart failure  Diagnosis Cardiac MRI: Characteristic enhancement of the myocardial wall and myocardial edema Endomyocardial biopsy: is the gold standard for diagnosis; however, it is rarely needed. Indications: Acute deterioration of cardiac function without a known etiology Failure to respond to therapy Findings: Cellular infiltrates may be: Lymphocytic, Eosinophilic, Neutrophilic, Mononuclear Myocyte necrosis Interstitial fibrosis Myofiber hypertrophy Granulomatous changes: Mycobacterium, Fungi, Parasitic, Sarcoid myocarditis (noncaseating) Giant cells: giant-cell myocarditis  Management General principles Supportive- mainstay of treatment, but often includes: Heart failure management Arrhythmia management Treating the underlying etiology (when possible)  Management – Heart Failure Medical therapy for heart failure: Diuretics ACE inhibitors Beta-adrenergic blockers Angiotensin II receptor blockers For fulminant (sudden/intense) heart failure: Intraaortic balloon pump Left ventricular assist device Cardiac transplantation  Arrythmia management & other considerations Arrhythmia management Antiarrhythmic therapy Cardioversion Temporary or permanent pacing Other considerations Anticoagulants are indicated for: Intracardiac thrombi Evidence of systemic embolism Atrial fibrillation Avoidance of: NSAIDs Alcohol consumption Exercise  Long term management Most patients will have a partial or full recovery. However, long-term follow-up and monitoring are recommended. Gradual resumption of physical activities Serial echocardiography monitoring Re-evaluation and titration of medications, as appropriate  Test yourself A patient recently diagnosed with pericarditis states he was “googling” the diagnosis and asks for your help in defining a pericardial friction rub. Which of the following is the most appropriate definition? A. Inflammation due to pericarditis causes the patient to rub their chest for pain relief. B. The fluid around the heart makes a splashing sound that can be heard on auscultation. C. The visceral pericardium and the parietal pericardium audibly rub against each other. D. Inflammation of the parietal pleura causes a rubbing sound. REVIEW:  Endocarditis overview Endocarditis is an inflammatory disease involving the inner lining (endocardium) of the heart, most commonly affecting the cardiac valves. Both infectious and noninfectious etiologies lead to vegetations on the valve leaflets. Patients may present with nonspecific symptoms such as fever and fatigue. Important clinical exam findings include a new or changed heart murmur and common extra-cardiac signs, such as Osler nodes, Janeway lesions, splinter hemorrhages, and Roth spots. The diagnosis is based on clinical findings, blood cultures, and echocardiography showing valvular vegetations. Management includes intravenous antibiotics for infectious cases, addressing the underlying etiology for noninfectious cases, and surgical repair when necessary.  Pericarditis overview Pericarditis is an inflammation of the pericardium, often with fluid accumulation. Acute pericarditis is usually idiopathic and manifests as fever, pleuritic chest pain, and an audible pericardial rub by auscultation. Diffuse upwardly concave ST-segment elevations in the initial ECG and pericardial effusion on echocardiography confirm the diagnosis. Acute pericarditis is usually self-limiting (2–6 weeks); therefore, management is conservative. Treatment depends on the cause, but general measures include analgesics, anti-inflammatory drugs, colchicine, and rarely surgery.  Overview of Pericardial effusion Pericardial effusion is the accumulation of excess fluid in the pericardial space around the heart. The pericardium does not easily expand; thus, rapid fluid accumulation leads to increased pressure around the heart. The increase in pressure restricts cardiac filling, resulting in decreased cardiac output and cardiac tamponade. Signs and symptoms usually occur in the setting of cardiac tamponade and include dyspnea, hypotension, muffled heart sounds, jugular venous distension, and pulsus paradoxus. The diagnosis of pericardial effusion is confirmed with echocardiography. Small effusions in stable patients are treated medically. Larger effusions and cardiac tamponade may require pericardiocentesis or pericardiotomy.  Myocarditis overview Myocarditis is an inflammatory disease of the myocardium, which may occur alone or in association with a systemic process. There are numerous etiologies of myocarditis, but all lead to inflammation and myocyte injury, most often leading to signs and symptoms of heart failure. The diagnosis is supported by clinical findings, laboratory evaluation, and cardiac imaging. A definitive diagnosis by endomyocardial biopsy is rarely required. Management is supportive and aimed at addressing complications. If we have time…  In –Class Activity Case HPI: 68-year-old Caucasian women with a PMH of Rheumatoid arthritis and a prosthetic aortic valve, who was brought to the emergency department (ED) after her family found her extremely lethargic and confused at home. She had been complaining of fevers, chills, headache, and neck pain for 2 days prior to presentation, and as per the patient’s family had steadily become less and less communicative. Otherwise, the patient has had no major medical issues in the last year since her aortic valve replacement. PMH: CAD, depression, type II DM, eczema, HTN, fibromyalgia, severe aortic stenosis with valve replacement Medications: Aspirin DR tablet 81 mg PO daily Atorvastatin 20 mg PO daily Fluoxetine 40 mg PO daily Glimepiride 4 mg PO daily Infliximab 3 mg/kg IV every 2 months Lisinopril 10 mg PO daily Pregabalin 75 mg PO BID Triamcinolone 0.1% lotion topical BID Vitamin D3 5,000 IU PO daily In –Class Activity Case Surgical History: Bioprosthetic aortic valve replacement (10 months ago), S2–S4 diskectomy (4 years ago), tubal ligation (>15 years ago), cholecystectomy (>15 years ago) Allergies: Hydrocodone/acetaminophen (vomiting) FH: Father passed away from HF; mother has type II DM, HTN, and h/o stroke; sister has type II DM, COPD, and HTN Social history: Widowed, lives by herself, never used alcohol, former smoker 1ppd (quit 10 years ago) Case Study: ROS Unable to obtain due to patient inability to communicate  Physical Examination Vital Signs: Temp 102.1°F (tympanic), HR 112 bpm, RR 19 breaths per minute, BP 91/52 mm Hg, SpO2 97% (on room air), Ht 165 cm, Wt 91 kg, BMI 33.4 kg/m2 General Lethargic, acutely ill appearing, appears stated age HEENT: Normocephalic, atraumatic, PERRLA, EOMI, faint conjunctival hemorrhage, non- icteric sclera, poor dentition, no erythema or swelling in the oropharynx Neck: No nuchal rigidity Pulmonary: Clear to auscultation bilaterally, no wheezes or crackles Cardiovascular: Regular rate and rhythm, faint systolic murmur over the right base Abdomen: Soft, non-distended, no masses, no focal rebound or guarding present. Neurology: AO × 1, no focal deficits, strength and sensation full and symmetric Extremities: Intact distal pulses, no LE edema Skin: Warm, diaphoretic. erythematous macular rashes distributed along the thenar and hypothenar eminences of both hands. Back: Tenderness to palpation on lower lumbar region