Case: Daphne Rogers — Cardiovascular Presentations and Clinical Reasoning

MICN 201, Integrated Cases, Tutorial 2. This tutorial is based on the case of Daphne Rogers, an 82-year-old woman with a complex cardiovascular presentation. We use this case to practise differential diagnosis construction, history-taking, examination findings, and investigation interpretation.

CASE SUMMARY

Daphne Rogers, 82-year-old retired school teacher, referred to the outpatient cardiology clinic by her GP for progressive fatigue, breathlessness on exertion (now limiting her to walking one block), occasional chest tightness, and two episodes of near-syncope (brief lightheadedness on standing and on climbing stairs). Background: known hypertension (on ramipril 10 mg), type 2 diabetes, hyperlipidaemia, previous smoker (40 pack-year history, stopped 15 years ago). No previous cardiac diagnoses.

On examination: BP 145/75, HR 82 and regular; JVP elevated 4 cm above the sternal angle; apex beat displaced and heaving; soft systolic murmur loudest at the right upper sternal edge, radiating to the carotids, grade 3/6; auscultation of lung bases — bibasal fine crackles; ankles show pitting oedema to the mid-calf.

DIFFERENTIAL DIAGNOSIS — APPROACH

The problem list: (1) Progressive dyspnoea on exertion; (2) Chest tightness; (3) Near-syncope; (4) Murmur — ejection systolic, radiating to carotids; (5) Signs of heart failure (elevated JVP, displaced heaving apex, crackles, oedema). Key differentials to consider:

(A) Aortic stenosis (AS): the most likely unifying diagnosis — ejection systolic murmur loudest at right upper sternal edge (RUSE) radiating to carotids; heaving non-displaced apex (LV pressure overload hypertrophy); the classic triad of AS symptoms: angina (chest tightness), syncope (on exertion — impaired cardiac output), and dyspnoea/heart failure. HFpEF (heart failure with preserved ejection fraction) due to concentric LVH from AS causes the signs of congestion. AS is common in the elderly (calcific/degenerative AS). Confirmed by echocardiography (valve area, peak gradient).

(B) Heart Failure: the signs are consistent with congestive cardiac failure (CCF) — elevated JVP (elevated RAP), bibasal crackles (pulmonary oedema), oedema. Could be: HFpEF (preserved EF, diastolic dysfunction — common in elderly hypertensive women, diabetes, concentric LVH); HFrEF (reduced EF, systolic dysfunction — if there is underlying IHD or dilated cardiomyopathy).

(C) Ischaemic Heart Disease (IHD): chest tightness + exertional dyspnoea in a patient with multiple cardiovascular risk factors (age, female post-menopause, hypertension, diabetes, hyperlipidaemia, ex-smoker — high Framingham risk). May coexist with AS. ACS would be more acute.

(D) Pulmonary hypertension: dyspnoea + near-syncope could suggest PAH, but the murmur pattern and heaving apex are not typical of RV hypertrophy; RV heave would be at the left sternal edge.

(E) Atrial fibrillation: excluded for now as HR is regular; but history of paroxysmal AF (palpitations, intermittent near-syncope) is possible.

CLINICAL REASONING FRAMEWORK

The structured clinical reasoning approach for SAQ-style questions: (1) Problem representation: "An 82-year-old woman with multiple cardiovascular risk factors presenting with the classic triad of aortic stenosis symptoms (exertional dyspnoea, chest pain, syncope) and a calcific ejection systolic murmur at the right upper sternal edge with signs of congestive heart failure." (2) Hypothesis generation: list differentials in order of probability. (3) Hypothesis refinement: identify which history, examination, and investigation findings support or refute each. (4) Investigation plan: targeted to confirm/exclude leading differentials. (5) Management plan: evidence-based.

INVESTIGATIONS

Bedside: ECG — may show LVH pattern (Sokolov-Lyon criteria: S in V1 + R in V5 or V6 > 35 mm; strain pattern — downsloping ST depression in lateral leads), signs of ischaemia. Bloods: FBC (anaemia can exacerbate HF), U&E (renal function — important before diuresis; hypokalaemia with diuretics), BNP/NT-proBNP (elevated in HF — marker of ventricular wall stress), troponin (if ACS suspected). Echocardiogram: key investigation — valve morphology and area (AVA <1.0 cm2 = severe AS), peak aortic valve gradient (>40 mmHg = severe), LV dimensions and EF (hypertrophy vs dilation), diastolic function, pulmonary artery pressure. Coronary angiography: if IHD suspected or before AVR (TAVI/SAVR — exclude significant CAD).

MANAGEMENT OF SEVERE AS WITH HEART FAILURE

There is no effective medical therapy for severe symptomatic AS to improve survival — diuretics for symptom management of congestion; avoid vasodilators (can cause haemodynamic collapse in fixed-output states). Definitive: valve replacement. In an 82-year-old with multiple comorbidities, TAVI (transcatheter aortic valve implantation) is preferred over surgical AVR (SAVR) — equivalent or superior outcomes in high-surgical-risk patients (PARTNER trial).