Case 06: Fainting

Professor Wilkins, a 68-year-old woman, presents with episodes of dizziness and a single episode of syncope (fainting) during exertion. She is known to have hypertension. On auscultation a harsh systolic murmur is heard, loudest at the right upper sternal border, radiating to the carotids. Her apex beat is forceful and sustained. Echocardiography confirms aortic stenosis.

Heart murmurs arise from turbulent blood flow: either through a narrowed (stenotic) valve or backwards through a leaky (regurgitant/incompetent) valve. Aortic stenosis produces a midsystolic murmur (beginning after S1, ending before S2) as blood is forced through the narrowed aortic valve during ventricular ejection. The murmur of mitral stenosis is diastolic — blood flows through the narrowed mitral valve during ventricular filling. Aortic incompetence produces an early diastolic murmur; mitral incompetence produces a pansystolic murmur.

In aortic stenosis, the left ventricle must generate higher pressures to eject blood through the narrowed valve (upstream effect). Over time this causes concentric left ventricular hypertrophy (LVH). The hypertrophied muscle has increased oxygen demand but receives inadequate coronary perfusion, especially on exertion, causing anginal chest pain. Downstream effects include restricted cardiac output, reduced cerebral perfusion (dizziness and syncope on exertion), and reduced coronary artery flow. The forceful or thrusting apex beat reflects the high-pressure LV contraction against the stenotic valve.

The classic symptom triad of severe aortic stenosis is chest pain (angina on exertion), syncope (exertional), and dyspnoea (from impaired cardiac output progressing to heart failure). Once symptoms develop, prognosis without intervention is poor (2–5 years median survival).

Rheumatic fever (RF) is a major cause of acquired valvular heart disease, particularly mitral stenosis. It predominantly affects Maori and Pacific children and young people aged 4–19 years in New Zealand. Group A streptococcal pharyngitis triggers an autoimmune response cross-reacting with cardiac proteins, causing pancarditis and valve scarring over time. The NZ guidelines for RF diagnosis have replaced the Jones criteria to account for higher pre-test probability in high-incidence regions and populations. Secondary prophylaxis with monthly intramuscular benzathine penicillin for 10 years or until age 21 prevents recurrent RF and further cardiac damage.

Normal arterial blood pressure in a healthy 20-year-old: systolic 110–120 mmHg, diastolic 70–80 mmHg, pulse pressure 30–50 mmHg. For a healthy 60-year-old: systolic 110–139 mmHg, diastolic 70–89 mmHg. The arterial pulse is a pressure wave propagated at 4–5 m/sec in young adults, rising to 10 m/sec with arterial stiffening in older age. The apex beat is the most lateral and inferior point of cardiac impulse, normally at the 5th intercostal space in the midclavicular line.

Heart sounds: S1 = closure of AV valves (mitral, tricuspid) at the start of systole; S2 = closure of semilunar valves (aortic, pulmonary) at the end of systole; S3 = rapid ventricular filling in early diastole (not normally heard in healthy adults); S4 = atrial contraction filling the ventricle (not normally heard in healthy adults).