Understanding Valve Disease

Valve Disease Overview

• Valve disease is characterized by four main types including stenosis, regurgitation, prolapse, and murmur.
• Nursing involves understanding valve function through diagnostic tests, clinical signs and symptoms, risk factors, and treatment options.

Normal Physiology

• Valves open and close depending on pressure differences in the atria and ventricles during the cardiac cycle.
• During cardiac diastole, the mitral and tricuspid valves open, allowing blood to flow from the atria to passively fill the ventricles; atrial systole then actively fills the ventricles.
• During ventricular systole, the ventricle walls contract and pressure rises, closing the mitral and tricuspid valves while the aortic and pulmonic valves open to eject blood.
• Heart sounds correlate with valve closures: S1 is the closure of mitral & tricuspid valves (lub), and S2 is the closure of the aortic & pulmonic valves (dub).
• Auscultation of heart valves requires knowledge of specific anatomical landmarks.

Terminology

• Stenosis refers to the narrowing of the valve opening restricting forward blood flow.
• Regurgitation is incomplete valve closure leading to backward blood flow.
• Prolapse is the buckling of valve leaflets, most often associated with the mitral valve.
• A murmur is a turbulent blood flow, graded on a scale from 1-6 (faint to loud);

Mitral Valve Stenosis (MS)

• MS is defined by a smaller valve opening that prevents complete emptying of the atrium into the ventricle during diastole.
• Thickening, stiffening, and shortening of leaflets due to scarring from inflammation occurs in MS.
• MS causes enlargement of the left atrium due to higher outflow pressures.
• MS results in a diastolic murmur as blood flow is turbulent across the stenotic valve during ventricular diastole.
• The most common etiology is Rheumatic Heart Disease; other causes include Radiation, Autoimmune (RA and SLE), and congenital valve abnormalities.
• Clinical manifestations include exertional dyspnea, loud S1, diastolic murmur, fatigue, palpitations, and hoarseness.

Mitral Valve Regurgitation (MR) and Prolapse (MVP)

• MR occurs when valve leaflets cannot completely close during systole, often due to fibrosis and calcification.
• In MR, LA enlargement, LV dilation & hypertrophy can result in decreased cardiac output.
• MVP involves leaflets that enlarge and buckle back into the left atrium during systole.

Mitral Valve Regurgitation and Prolapse (MVP)

• Mitral valve prolapse can cause Mitral Regurgitation.
• Etiologies include conditions such as rheumatic heart disease, acute myocardial infarction (AMI), and infective endocarditis.
• Regurgitation presents as a systolic murmur and palpitations, and can lead to acute pulmonary edema, cardiogenic shock, chronic exertional dyspnea, orthopnea, fatigue, and elevated S3.
• Mitral valve prolapse can be asymptomatic but may cause palpitations, dyspnea, dizziness, chest pain not responsive to nitrates, and activity intolerance.

Aortic Valve Stenosis

• In Aortic Stenosis, leaflets stiffen, narrow, and retract, which is often compounded by calcification, causing an obstruction to LV outflow.
• The increased afterload from Aortic Stenosis leads to LV hypertrophy, eventually progressing to LV failure.
• Aortic Valve Stenosis results in a systolic murmur due to increased turbulent blood flow.
• Commonly caused by congenital valve abnormality, rheumatic fever, or degeneration.
• Clinical manifestations are systolic murmur, decreased exercise tolerance with dizziness/lightheadedness, angina, syncope, or exertional dyspnea.
• Nitroglycerin is contraindicated because it reduces preload.

Aortic Valve Regurgitation

• Aortic Valve Regurgitation is caused by leaflets unable to close completely which overloads the LV, resulting in dilation and hypertrophy.
• Characterized by a diastolic murmur as blood regurgitates backward during ventricular diastole.
• Potential causes include rheumatic heart disease, congenital valve abnormality, infective endocarditis and aortic dissection.
• Patients are generally asymptomatic for many years.
• Symptoms are diastolic murmur, S3 or S4 heart sounds in acute cases, and if chronic, exertional dyspnea, fatigue, and angina

Diagnostics and Treatment

• Echocardiograms (transthoracic and transesophageal) with Doppler color-flow imaging are used for diagnosis.
• A chest X-ray helps visualize valve calcification, while a 12-lead ECG may provide additional information.
• Cardiac catheterization is completed to measure actual pressure gradients across the valve when surgical intervention is required.
• Conservative treatment includes managing symptoms of heart failure, pulmonary edema, fatigue, and dysrhythmias.
• Medications such as vasodilators, beta blockers, diuretics, ACE inhibitors, inotropes (Digoxin), antibiotics, and anticoagulants such as warfarin are considered.
• Lifestyle guidance may include prophylactic use of antibiotics, adherence to prescribed medications, avoiding caffeine and OTC stimulants, and being aware of emergency warning signs.

Catheter and Surgical Interventions

• Catheter-based interventions include balloon valvuloplasty and mitral clip.
• Valve replacement or repair are the main surgical interventions; annuloplasty rings are used to strengthen the mitral valve repair.

Venous Thromboembolism (VTE) & Pulmonary Embolism (PE)

• VTE is formation of a thrombus that can occur in superficial or deep veins.
• Superficial vein thrombosis manifests as palpable, painful, firm and cordlike engorged vein.
• DVT presents as unilateral edema, pain, dilated superficial veins, with possible paresthesias.
• Complications of DVT are PE and Postthrombotic syndrome.
• PE is a blockage of 1 or more pulmonary arteries by a thrombus, fat or air embolus, or tumor tissue.
• VTE can lead to PE and describe spectrum from DVT to PE.
• The goal includes prevention and prophylaxis and to be based on bleeding risk and thrombosis.
• The clinical manifestations in PE includes dyspnea, cough with potential hemoptysis, chest pain, crackles, wheezing, tachycardia, syncope, and a pulmonic heart sound.
• Diagnostics for PE include D-dimer, CTA, ventilation-perfusion scan, ECG and blood gases.
• Treatment includes anticoagulation therapy and may require fibrinolytics or surgical therapy.

Virchow's Triad

• Virchow's Triad (venous stasis, endothelial damage, hypercoagulability) are the three factors that that cause venous thrombosis.
• Venous stasis risk factors: dysfunctional valves, inactive extremity muscles, obesity, pregnancy, chronic HF or atrial fibrillation, traveling on long trips, surgery, prolonged immobility.
• Endothelial damage can be caused directly (surgery, burns, catheters, trauma) or indirectly (chemotherapy, diabetes, sepsis.)
• Hypercoagulability results from smoking, oral contraceptives, hormone replacement therapy, age >35 years, family history of VTE or cancer.

VTE Interprofessional Care

• The focus on care is prevention, intervention is based on bleeding and thrombosis risks, medical history, current drugs, and potential diagnoses.
• Measures include early mobilization, compression stockings and intermittent pneumatic compression devices (IPCs).
• VTE prophylaxis uses anticoagulants to prevent clot formation with Vitamin K antagonists, thrombin inhibitors, or factor Xa inhibitors.
• Low risk VTEs receive no intervention, moderate risk VTEs receive UH or LMWH and high risks receive trauma abdominal/pelvic surgery.