Heart Layers and Acute Pericarditis

Layers of the Heart

• The heart has three layers: the pericardium, the myocardium, and the endocardium.
• The pericardium has fibrous, serous parietal, and serous visceral (epicardium) layers.

Acute Pericarditis

• Acute pericarditis involves inflammation of the pericardial sac.
• Etiology can be idiopathic, infectious, noninfectious, or autoimmune.
• Infectious causes include viral, bacterial, fungal, and parasitic infections.
• Noninfectious causes include AMI, renal failure, certain cancers, trauma, radiation, myxedema, and dissecting aortic aneurysm.
• Autoimmune causes include Dressler's syndrome, post-pericardiotomy syndrome, rheumatic fever, and rheumatic diseases like RA, SLE, scleroderma, and ankylosing spondylitis.

Pathophysiology of Pericarditis

• An acute inflammatory response results in an influx of neutrophils, leakage of fluid into the pericardial sac, increased pericardial vascularity, and fibrin deposition on the epicardial surface.
• Subacute pericarditis occurs weeks to months after a precipitating event (Dressler Syndrome).
• Chronic pericarditis lasts longer than 6 months.
• The heart no longer moves smoothly within the pericardial sac, creating friction and adhesions.

Clinical Manifestations of Pericarditis

• Progressive, severe chest pain worsens with deep inspiration and when lying flat and is relieved when sitting up and leaning forward and can refer pain to the shoulder and upper back.
• Other symptoms include fever, tachypnea, dyspnea, and anxiety.
• A hallmark finding is a pericardial friction rub, which is a scratchy, grating, high-pitched sound heard best at the left lower sternal border.

Diagnostics for Pericarditis

• ECG shows global ST elevation.
• Echocardiogram assesses for effusion or tamponade.
• CXR, CT, or MRI visualizes the pericardial sac and assesses space for size.
• Lab work includes CBC, CRP, sed rate, and troponin levels.
• Pericardiocentesis involves the analysis of the pericardial fluid.

Complications of Pericarditis

• Pericardial effusion refers to excess fluid in the sac, leading to muffled heart sounds and potential compression of the heart and nearby structures.
• Compression can cause hiccups (phrenic nerve compression), hoarseness (laryngeal nerve compression), and lung issues such as cough, SOB, and increased respiratory rate.
• Cardiac tamponade involves decreased diastolic filling, resulting in decreased cardiac output with pulsus paradoxus, and decreased SBP with inspiration.
• Cardiac tamponade requires urgent pericardiocentesis.
• Beck's Triad: narrow pulse pressure, muffled heart sounds, JVD

Interprofessional Care for Pericarditis

• Treatments include antibiotics (if infective), NSAIDs, and corticosteroids.
• Colchicine inhibits neutrophil migration into areas of inflammation.
• O2, Bedrest, and Positioning is needed
• Uremic pericarditis is treated with dialysis.
• Prevent immobility complications.
• Provide psychological support.
• Surgical interventions include pericardiocentesis and creating a pericardial window to drain fluid into the pleural cavity.

Pericardiocentesis Complications

• Pericardiocentesis is indicated for cardiac tamponade, purulent pericarditis, and malignancy.
• Percutaneous, echocardiogram guided
• Potential complications include dysrhythmias, cardiac tamponade, pneumomediastinum, pneumothorax, and myocardial or coronary artery laceration.

Chronic Constrictive Pericarditis

• Fibrosis, rigidity, and thickening of the pericardium lead to decreased elasticity and restricted ventricular filling, reducing cardiac output.
• The pericardial space gets destroyed.
• Etiologies include tuberculosis, heart surgery, radiation therapy, and idiopathic causes.
• Clinical manifestations are similar to HF and cor pulmonale, including DOE, peripheral edema, ascites, JVD, fatigue, anorexia, and weight loss.
• Treatment include pericardiectomy and diuretics.
• Diagnostics include echo, CT, MRI

Acute Myocarditis

• Acute myocarditis involves focal or diffuse inflammation of the myocardium.
• Etiology includes infectious causes like viral, bacterial, and fungal infections, as well as noninfectious causes like radiation, pharmacologic agents, and chemical factors, also idiopathic causes.

Pathophysiology of Myocarditis

• Causative agents invade the myocardium, damaging myocytes.
• The immune response releases cytokines and free radicals.
• Autoimmune responses activate inflammation against self, leading to necrosis.

Clinical Manifestations of Myocarditis

• Early symptoms resemble viral infections and include fever, fatigue, myalgia, pharyngitis, and lymphadenopathy.
• Cardiac signs appear 7-10 days after the causative agent and include pericarditis (pleuritic chest pain, pericardial rub) and pericardial effusion.
• Late cardiac signs indicate heart failure or AMI with S3 sounds, crackles or rhonchi, and peripheral edema with JVD.

Diagnostic Testing for Myocarditis

• ECG shows diffuse ST segment changes, dysrhythmias, and conduction abnormalities.
• Echocardiogram assesses effusion or tamponade.
• CBC, sed rate, CRP, viral titers, and troponin levels are measured.
• Troponin will be elevated similar to a heart attack
• Pericardial fluid sample and endomyocardial biopsy may be performed.

Complications of Myocarditis

• Decreased cardiac output can result in severe heart failure and dilated cardiomyopathy.
• Severe heart failure may require intra-aortic balloon pump, left ventricular assist device, or heart transplant.
• Sudden cardiac death from dysrhythmias r/t conduction abnormalities, heart failure

Interprofessional Care for Myocarditis

• Supportive care includes oxygen therapy, bed rest with alternating activity, a quiet environment, semi-Fowler's position, and anxiety management.
• Medications include ACE inhibitors, beta-blockers, diuretics (for heart failure), digoxin, anticoagulants (for clot prevention), immunosuppressive agents, or antivirals.

Infective Endocarditis (IE)

• IE involves infection of the endocardium and cardiac valves.
• Etiology includes bacterial, viral, or fungal pathogens, with Staph aureus, strep viridans, coagulase negative staph, and HACEK organisms being common culprits.
• Acute manifestations - rapid valvular dysfunction.
• Subacute manifestations - pre existing valve disease with clinical course extends over months

Risk Factors for IE

• Risk factors include previous IE, IV drug abuse, calcific heart valves, previous valve replacement, invasive procedures (pacemaker insertion, dialysis, central lines, surgery), and recent dental surgery.

Pathophysiology for IE

• The condition progresses through three stages: bacteremia, adhesion, and vegetation.
• Damage to the endothelium enables attachment of infective organisms.
• Vegetation: Fibrin, leukocytes, platelets, and microbes stick to the valve or endocardium
• Parts break off and enter circulation (embolization)
• Left-sided vegetation can move to brain, kidneys, spleen, and extremities
• Right-sided vegetation can move to lungs (PE)

Clinical Manifestations of IE

• Clinical manifestations are nonspecific and may involve multiple organ systems.
• Acute symptoms include weakness, malaise, fatigue, myalgia, and low-grade fever.
• Subacute symptoms include arthralgia, back pain, abdominal discomfort, anorexia, headache, and finger clubbing.
• Vascular signs include splinter hemorrhages, petechiae, Osler's nodes, Janeway's lesions, and Roth's spots.
• Septic emboli lead to neuropathic, organ-specific pain from ischemia.
• Heart failure results in cough, DOE, and orthopnea. New or changing systolic murmur

Diagnostic Testing for IE

• Health history is important to gather.
• Diagnostic testing involves laboratory testing, including blood cultures (3 from different sites over 30min-1hour period).
• Include ESR and CRP, and CBC with differential to measure mild leukocytosis.
• Echocardiogram assesses valvular function and detects vegetation.
• Duke criteria = Major blood culture and organism, new vegetation.
• Duke criteria = Minor: IVDA, vascular symptoms, ECHO findings

Complications of IE

• Systemic embolization occurs when parts of the fragile vegetations break off, causing a shower of emboli.
• Left sided vegetations - brain, kidneys, spleen, extremities
• Right sided vegetations - lungs
• Valve damage leads to dysrhythmias and heart failure.
• Myocardium invasion
• Heart failure (80% with aortic valve involvement, 50% with mitral valve involvement).
• Also sepsis and heart block

Interprofessional Care for IE

• Give prophylaxis with antibiotics for prevention who are at risk.
• Prosthetic heart valves, congenital heart disease, previous endocarditis
• Dental procedures, respiratory tract incisions, tonsillectomy and adenoidectomy, some surgical procedures
• Antibiotics are given based on blood culture results until repeats are negative.
• Long-term (4-6 weeks) IV antibiotics, often via midline or PICC.
• Include follow-up diagnostics with ECHO and inflammatory markers.
• Supportive care with antipyretics, fluids, and rest.
• Valve replacement.

Rheumatic Heart Disease

• Rheumatic fever (RF) is a delayed complication following a Group A streptococcal pharyngeal infection ("strep throat").
• Involves an abnormal immunologic response to Strep cell membrane antigen.
• Is caused by the acute, inflammatory process of rheumatic fever (RF)
• The disease causes permanent scarring and deformed heart valves (aortic & mitral).

Effects of Rheumatic Fever

• Rheumatic fever affects all layers of the myocardium, also known as pancarditis.
• The effects on the endocardium include swelling and erosion of valve leaflets and vegetations.
• Calcification = stenosis
• Inability to close (stiff) = regurgitation
• The effects on the myocardium is scar tissue from Aschoff's bodies.
• The the effects on the pericardium is pericarditis, pericardial effusion, potential constrictive pericarditis.

Clinical Manifestations of Rheumatic Heart Disease

• It involves joint pain with Arthritis
• Also, Carditis and Pancarditis
• Heart murmur, Cardiomegaly and HF, Pericarditis (friction rub or effusion)
• Develop subcutaneous nodules
• Erythema Marginatum which is Bright pink, nonpruritic, maplike macular lesions
• There is also Sydenham Chorea which involved involuntary movement, weakness, changes to speech and gait
• Anamnesis = "A history of"

Diagnostic Studies for Rheumatic Fever

• Early detection is key with rheumatic heart disease
• Requires Recognition and treatment of Group A beta strep pharyngitis
• With Prophylactic Abx treatment for those with prior RF (q3-4w IM injection)
• Requires a History and Physical examination
• And, Lab work – CBC, ESR, CRP, bacterial culture/ rapid strep test
• Imaging: Echocardiogram – confirms valvular dysfunction
• Chest X-ray – cardiomegaly
• ECG: prolonged PR interval (>0.20)

Nursing Care for Rheumatic Fever

• Provide medications: Abx: penicillins, cephalosporins, macrolides (azithromycin, etc.)
• Anti-inflammatories: salicylates, NSAIDS, and corticosteroids
• Requires Bed rest or limited activity
• Treat symptoms: Fever management and heat for painful joints