Please enable JavaScript.
Coggle requires JavaScript to display documents.
Inflammatory Heart Disorder - Coggle Diagram
Inflammatory Heart Disorder
Myocarditis
Definition
Inflammation of the myocardium (heart muscle), which can affect the heart’s electrical system, reducing its ability to pump blood and leading to heart failure, arrhythmias, or sudden death
Occur with no symptoms and can remain undiagnosed
Incidences: more common in men than women
Etiology
Cause is unknown or idiopathic when no clear infection or trigger is identified
Non-Infectious Cause
Related to autoimmune, toxic, or hypersensitivity reactions
Autoimmune diseases
Systemic lupus erythematosus (SLE) ,Rheumatic fever, Sarcoidosis Giant cell
Toxins and drugs
Alcohol abuse, Cocaine, Chemotherapy agents (e.g., anthracyclines like doxorubicin), Radiation therapy, Environmental toxins (e.g., heavy metals)
Medications
Certain antibiotics (e.g., penicillin, sulfonamides), Vaccines (rare cases, such as the smallpox vaccine), Immunotherapy drugs
Pathophysiology
Left Ventricular End-Diastolic Volume (LVEDV) refers to the amount of blood in the left ventricle at the end of diastole (the heart's relaxation phase, just before it contracts)
An inflammation of the heart muscle (myocardium), changes in LVEDV can provide important information about the heart's function and the disease's impact on cardiac output
Left Atrial Pressure (LAP) refers to the pressure in the left atrium of the heart ,(cause pulmonary circulation backward)
Clinical Manifestations
Investigations
Cardiac markers (↑creatinine kinase, troponin T, CPK levels)
Myocardial cell damage
ECG
Non-specific ST segment and T wave changes, atrial / ventricular arrhythmias, heart block, Sinus tachycardia
Blood test (FBC: ↑WBC, ↑ESR-,↑CRP)
Indicates general inflammation in the body
CXR
To determine the size and shape of the heart i.e. cardiomegaly, pleural effusion pulmonary oedema
Physical examination
Abnormal heartbeat, Fever , Tachycardia, Oedema in the leg
Echocardiogram
Heart muscle damage
Patient's history
Endomyocardial biopsy
To identify patchy cell necrosis and inflammatory process for definitive diagnosis
Risk Factors
Altered immune response i.e. malnutrition, alcoholism, immunosuppressive drugs, exposure to radiation, stress, advanced age
Complication of rheumatic fever and pericarditis
Complication
Ventricular tachyarrhythmias
Dilated cardiomyopathy
Atrial fibrillation
Sudden cardiac death
Multisystem organ failure
Management
Cardiac drugs
Beta blockers
Management of hypertension, arrhythmias, heart failure, and after heart attacks
Examples : Metoprolol, Atenolol, Carvedilol, Bisoprolol
Angiotensin receptor blocking agents
Used in patients who cannot tolerate ACE inhibitors due to side effects like cough
Examples: Losartan, Valsartan, Candesartan
ACE Inhibitors
To treat conditions like hypertension, heart failure, and postmyocardial infarction (heart attack)
Examples : Lisinopril ,Enalapril ,Ramipril,Captopril
Immunosuppressive therapy with corticosteroid
To reduce inflammation
i.e. Gamma globulin
Antibiotic therapy
To treat infection
Anti arrhythmia agent
i.e. Amiodarone
Diuretics
To treat fluid overload
Anticoagulants
Warfarin (Coumadin), Enoxaparin (Lovenox), Fondaparinux (Arixtra)
Behavioural changes
i.e. Rest, fluid restriction, low salt diet
Nursing Care
Monitoring of vital signs (TPR & BP) & dysrhythmias
Provide oxygen therapy when necessary
Patients with dysrhythmias - Continuous cardiac monitoring
Assess for signs and symptoms of heart failure
Monitor level of pain
Use elastic pressure stockings (TEDS); encourage active and passive exercise
Provide emotional support and relieve anxiety
Prognosis
Complete recovery
Approximately half recover without any residual cardiac effect
Incomplete recovery
If extensive myocardial damage when necrotic tissue replaced with scar tissue resulting in residual defects
Prevention
Nursing Diagnoses
Fatigue RT inflammation and impaired cardiac output
Anxiety RT possible long-term effects of the disorder
Decreased cardiac output RT myocardial inflammation
Excess fluid volume RT compensatory mechanism for decreased cardiac output
Pericarditis
Definition
Inflammation of the pericardium with presence of a thin fluid filled sac surrounding heart
Incidence
Acute or chronic and may involve fluid accumulation (pericardial effusion) or thickening of the pericardium
Primary or secondary to a cardiac or systematic disorder
In men < 50 years
Cause of Pericarditis
Classification
Clinical
Subacute pericarditis
6 weeks - 6 months
Chronic pericarditis
6 months
Acute pericarditis
< 6 weeks
Etiologic
Infectious
Viral, pyogenic, tuberculosis, fungal
Non-infectious
Uraemia, transmural myocardial infarct, neoplasm, idiopathic
Autoimmune
Rheumatic fever, rheumatic arthritis, Systemic lupus erythematosus (SLE), post traumatic
Pathophysiology
Clinical Manifestations
Chest pain
Precordial /retrosternal chest pain
Abrupt onset, sharp, steady or intermittent, radiate to the back / neck , ↑ with deep inspiration/ cough, change in body position or swallowing worsens with deep breaths or lying down and improves when sitting up or leaning forward
Main characteristic, heard on expiration
Leathery grating sound (inflamed pericardial layers rub against chest wall/pleural)
Fever
Low-grade fever may accompany the inflammation
Fatigue
General feeling of tiredness and malaise
Shortness of Breath
Especially when reclining due to pressure on the lungs
Palpitations
Sensation of a racing or fluttering heart
Investigation
ECG
Diffuse ST elevation PR depression
Echocardiogram
To assess heart motion & extent of restriction; ↑PA PVP
Cardiac enzymes
↑ troponin-to rule out myocardial infarction
PA PVP
Pericardial Aneurysm Pericardiocentesis Volume of Pericardial Fluid
Used in the context of assessing and managing pericardial effusions, particularly in patients with pericarditis or other related cardiac conditions
CXR
Cardiac enlargement, pericardial effusion
Cardiac CT or MRI
To identify pericardial effusion or constrictive pericarditis
CBC
↑WBC & ESR > 20mm/h → acute inflammation
Management
Proton pump inhibitors
To prevent peptic ulcers
Corticosteroid therapy
To suppress inflammatory response
NSAIDS (Indomethacin & Ibuprofen)
To reduce inflammation and relieve chest pain
Invasive Procedure
Pericardiocentesis
To remove fluid from pericardial sac
Partial or total pericardiectomy
To remove part or total pericardium to relieve ventricular compression and allow adequate filling
Aspirin & Acetaminophen
To reduce fever
Complications
Cardiac tamponade
Fluid ++ in pericardium→ pressure ++ on heart, prevent it from filling with blood → fatal ↓BP if untreated
Chronic constrictive pericarditis
Permanent thickening and scarring of the pericardium → hardening of tissues and restricts heart from working properly→ peripheral oedema & shortness of breath
Pericardial effusion
Abnormal collection of fluid between pericardial layers
Nursing Care
Nurse in Semi-Fowler’s position to facilitate breathing and relieve pain
Encourage deep breathing exercises (DBE) and use of incentive spirometry to promote ventilation
Administer prescribed medications (antibiotics, analgesics, anti inflammatories, NSAIDs, corticosteroids)
Maintain a quiet environment, advise gradual increment in daily activities, and plan nursing care to allow adequate rest and minimize O2 usage/cardiac workload
Administer O2 as necessary and maintain O2 saturation ≥ 95%
Assess hemodynamic status at least 3-4 hourly (vital signs, respiratory patterns, O2 saturation, cardiac rhythm & sounds, pain scale, urine output)
Nursing Diagnosis
Ineffective breathing pattern RT decreased lung capacity as evidence by c/o shortness of breath
Activity intolerance RT decrease cardiac output as evidenced by c/o weakness
Acute pain RT pleural membrane inflammation as evidence by c/o sharp persistent chest pain
Anxiety RT therapeutic interventions and uncertainty of prognosis as evidenced by verbalisation
Alteration in body temperature: Hyperthermia RT infection as evidenced by temperature of 37.5 to 38 C
Risk for decreased cardiac output
Health Education
Importance of continuing anti-inflammatory medications
NSAIDs need to take with food, milk, or Antacids
Rational
NSAIDs can cause irritation of the stomach lining, leading to gastritis or peptic ulcers. These can provide a protective barrier and help to buffer the stomach acid, reducing the risk of irritation
Medication such as antacids can neutralize stomach acid, further protecting the gastric mucosa and potentially reducing the risk of ulcers
Prescribe medications, its dose, effect, adverse effects and interactions
Monitoring weight twice weekly as NSAIDS may cause fluid retention
Rational
When these prostaglandins are inhibited, this can impair the kidneys' ability to filter waste and excrete excess fluid
NSAIDs may also cause the kidneys to retain sodium, leading to increased fluid volume in the body
NSAIDs can affect kidney function by inhibiting the production of prostaglandins and help maintain renal blood flow and promote the excretion of sodium and water
Maintain fluid intake at least 2500ml/day to ↓risk of renal toxicity due to NSAIDS use
Rational
Sufficient hydration promotes diuresis (the production of urine), which aids in the elimination of toxins and metabolites that could otherwise accumulate and cause kidney injury
NSAIDs can lead to fluid retention and altered renal function, increasing the risk of dehydration, especially in vulnerable populations such as the elderly or those with pre-existing renal conditions
Measures to maintain activity restriction → gradual increase when inflammatory resolved
Rational
Gradual activity restrictions provide the body with the necessary time to repair damaged tissues and return to a non-inflamed state
Monitor for s/s of recurrence → report to Dr promptly
Engaging in high-impact or strenuous activities too soon can exacerbate inflammation and lead to a longer recovery period or even chronic issues