A nurse is collecting data on a client who has valvular heart disease. Which of the following manifestations should the nurse anticipate? (Select All that Apply.)

Valvular heart disease involves structural damage to cardiac valves, impairing forward flow through stenotic orifices or permitting backward leakage via regurgitant leaflets. These mechanical defects disrupt normal laminar blood flow, generating turbulent currents that present as a audible heart murmur. The resulting hemodynamic strain elevates intracardiac pressures, causing myocardial ischemia, chest pain, and atrial dilation that triggers palpitations. A. Heart murmur: Mechanical valvular incompetence or restricted luminal narrowing disrupts smooth, laminar blood flow through the cardiac chambers. This structural turbulence creates audible acoustic vibrations during specific phases of the cardiac cycle. It remains the definitive clinical hallmark of valvular structural dysfunction. B. Abdominal pain: Visceral abdominal discomfort is not a direct or standard physiological consequence of localized cardiac valvular lesions. While advanced right-sided heart failure can cause congestive hepatomegaly, isolated valvular disease does not primarily present with acute abdominal distress. The symptom lacks direct pathophysiological alignment. C. Chest pain: Stenotic or regurgitant lesions increase ventricular workload, raising myocardial wall tension and oxygen demand while reducing coronary perfusion pressures. This supply-demand mismatch induces subendocardial ischemia, presenting as classic anginal discomfort. It signifies advanced hemodynamic strain on the myocardium. D. Palpitations: Valvular dysfunction expands atrial and ventricular chambers, stretching the conduction fibers and triggering ectopic foci or tachyarrhythmias like atrial fibrillation. Patients perceive these irregular, rapid contractions as a fluttering or thumping sensation in the chest. It reflects compromised myocardial electrical stability. E. Varicose veins: Superficial venous dilatation in the lower extremities stems from localized venous valvular incompetence and elevated hydrostatic pressures within the peripheral venous system. This peripheral vascular pathology runs entirely independently of central cardiac valvular hemodynamics. It does not map to intracardiac structural defects.