CFB MED05 Cardiovascular (i) Physical Examination (history Taking)
Cardiovascular history taking is the systematic collection of a patient's symptoms, risk factors, and relevant medical background—including chest pain, dyspnea, palpitations, syncope, and peripheral edema—to guide the clinical assessment of heart and vascular disease.
Cardiovascular System: History Taking for Cardiac Disease
The Big Idea: Before any ECG, echo, or catheterization, the history is the single most powerful diagnostic tool in cardiovascular medicine. A structured cardiovascular history — built around the cardinal symptoms of chest pain, dyspnoea, palpitation, syncope, and oedema — can correctly identify the diagnosis in the majority of cardiac patients. As Paul Wood (1950) warned: "We are in danger of losing our clinical heritage and pinning too much faith in figures thrown up by machines." [1]
Learning Objectives (derived from the lecture):
- Master the structure of a cardiovascular history (PC → HPC → PMH → DHx → FHx → SHx → Systemic Enquiry)
- Characterize each cardinal cardiac symptom using systematic frameworks (SOCRATES for pain)
- Differentiate cardiac from non-cardiac causes of each symptom using history alone
- Classify severity of angina (CCS classification) and heart failure (NYHA classification)
- Distinguish stable angina, unstable angina, and acute MI by history
- Identify "atypical" presentations and silent ischaemia
- Understand the mechanisms of cardiac dyspnoea from first principles
- Differentiate syncope from seizures by clinical features
- Integrate risk factors, drug history, family history, and social history into the cardiovascular assessment
1. Structure of the Cardiovascular History
The cardiac history follows the universal medical history structure but with specific emphasis on cardiovascular symptoms, risk factors, and drug history. [1]
The symptom that prompts the patient to seek medical attention — commonly chest pain, breathlessness (dyspnoea), palpitation, dizziness or blackouts (syncope). [1]
Record it in the patient's own words. Don't interpret it yet.
This should define the nature of the symptoms, initially through open questioning. Closed questions are used to elicit the presence or absence of features which help to differentiate between diagnoses. [1]
Systematic HPC Framework (from the lecture): [1]
| Element | What to Ask | Why It Matters |
|---|---|---|
| Onset | When did it start? Acute or gradual? | Acute onset → MI, PE, dissection, pneumothorax. Gradual → angina, HF |
| Duration | Minutes / hours / days / weeks | Angina = 2-10 min; MI > 30 min; musculoskeletal = hours |
| Severity | Scale of 0-10 | Helps triage and track response to treatment |
| Course | Worsening, improving, fluctuating? | Progressive worsening → unstable angina, decompensating HF |
| Intermittent or continuous | Always present or comes and goes? | Constant pain for hours ≠ typical angina |
| Precipitating factors | Obvious triggers? | Exertion → angina; lying flat → orthopnoea; emotion → arrhythmia |
| Relieving factors | What makes it better? | Rest/GTN → angina; sitting up → HF; NSAIDs → pericarditis |
| Associated features | Other symptoms? | Nausea/vomiting → MI; pink frothy sputum → pulmonary oedema |
| Previous episodes | Has this happened before? | Recurrent episodes suggest chronic condition |
Common symptoms associated with heart diseases: [1]
- Chest pain – SOCRATES
- Dyspnoea – exertional / orthopnoea / paroxysmal nocturnal dyspnoea
- Palpitations – ask patient to tap out the rhythm
- Syncope / dizziness – postural / exertional / random
- Oedema – peripheral oedema (e.g. lower limbs) / sacral oedema
- Intermittent claudication – e.g. leg pain worsened on exertion / improved at rest
- Systemic symptoms – fatigue / fever / weight loss / weight gain
2. Chest Pain (The First Cardinal Symptom)
If pain is a symptom, clarify the details using SOCRATES: [1]
| Letter | Full | Specific to Cardiac Pain |
|---|---|---|
| S | Site | Retrosternal or slightly left of sternum |
| O | Onset | Gradual build-up over 1-2 minutes (angina); rapid (MI); very sudden (dissection) |
| C | Character | Tightness, pressure, squeezing, heaviness, burning — NOT sharp/stabbing |
| R | Radiation | Neck, jaw, left shoulder/arm (ulnar distribution), occasionally right arm, interscapular, epigastrium |
| A | Associations | SOB, dizziness, syncope, diaphoresis, nausea |
| T | Time course | 2-10 min (angina); > 30 min (MI); worsening/improving/fluctuating |
| E | Exacerbating/Relieving | 4 "E"s aggravate angina; rest/GTN relieve angina; NSAIDs relieve pericarditis |
| S | Severity | Mild-moderate (angina); usually severe (MI); very severe (dissection) |
Chest pain or discomfort branches into: [1]
- Ischaemic chest pain (Angina pectoris)
- Stable angina
- Unstable angina
- Acute MI
- Other causes
- Atypical chest pain
High Yield: Angina Characteristics
Quality: Tightness, pressure, squeezing, heaviness, burning, aching, fullness, "heavy weight" or "band across chest" [1]
Location: Retrosternal or slightly to the left, occasionally at extrathoracic sites [1]
Radiation: Neck, throat, lower jaw, left shoulder or arm (ulnar distribution), occasionally right arm, interscapular, epigastrium or back [1]
Mode of onset and duration: Gradual increase and fading away, usually 2-10 minutes [1]
Aggravating factors — the 4 "E"s: Eating, Exertion, Emotion, Environment (hot or cold) [1]
Relieving factors: Rest, cessation of activity/stress, GTN (nitroglycerin) [1]
Associated symptoms: Shortness of breath, dizziness, syncope [1]
Why angina has these features (first principles):
- Angina results from an imbalance between myocardial oxygen supply and demand. The coronary arteries have a fixed stenosis, so when demand increases (exertion, eating, emotion, cold), supply cannot keep up → ischaemia → visceral pain.
- The pain is visceral (from the myocardium), which is why it is diffuse, poorly localized, and described as "pressure" rather than sharp. Visceral afferents travel via cardiac sympathetic nerves to spinal cord segments T1-T5, which also receive somatic afferents from the arm and jaw — this is why angina radiates to these areas (referred pain via convergence-projection theory).
- The pain fades with rest because demand decreases, and the stenotic but still patent artery can meet the reduced oxygen need.
- GTN works by venodilation (reducing preload and thus myocardial wall stress/demand) and some coronary vasodilation.
Why diabetics get silent ischaemia: Diabetic autonomic neuropathy damages the cardiac afferent nerve fibres, so the brain never receives the pain signal even though the myocardium is ischaemic. This is why DM patients can present with "painless MI" — they may only have breathlessness, nausea, or diaphoresis.
This is a critical distinction tested in exams. The three represent a spectrum of ischaemic heart disease with increasing severity. [1]
| Feature | Stable Angina | Unstable Angina | Acute MI |
|---|---|---|---|
| Trigger | 4 "E"s (predictable threshold) | Lower threshold or at rest | Usually spontaneous |
| Duration | < 2-10 minutes | < 20 minutes | > 30 minutes |
| Severity | Predictable, reproducible | More severe, escalating | Most severe |
| Response to rest/GTN | Relieved | May not be fully relieved | Not relieved |
| Associated symptoms | Usually just SOB | — | SOB, nausea, vomiting, diaphoresis, anxiety |
| Mechanism | Fixed stenosis; demand > supply | Plaque instability ± thrombus; partial occlusion | Complete thrombotic occlusion of coronary artery |
The underlying mechanism is an imbalance between blood supply and demand: [1]
- Coronary artery stenosis
- Coronary spasm
- Anaemia, thyrotoxicosis (increased demand with normal arteries)
- Aortic stenosis, hypertension (increased afterload → increased demand)
This functional classification grades the severity of stable angina based on the level of exertion that provokes symptoms. [1]
| Grade | Description |
|---|---|
| I | Angina only with strenuous, rapid, or prolonged exertion. Ordinary activities (walking, climbing stairs) do NOT cause angina |
| II | Slight limitation. Angina with walking/climbing stairs rapidly, walking uphill, walking after meals, in cold/wind, or under emotional stress, or only in the few hours after awakening |
| III | Marked limitation. Angina walking 1-2 blocks on level ground or climbing < 1 flight of stairs in normal conditions |
| IV | Inability to carry on any physical activity without discomfort; angina may be present at rest |
Why this matters clinically: CCS grade determines management intensity. Grade I-II patients may be managed medically. Grade III-IV patients need more aggressive investigation (stress testing, coronary angiography) and may need revascularisation. The concept of "unstable angina" includes new-onset angina of at least CCS class III severity, or crescendo angina increasing by ≥1 CCS class to at least class III. [1]
From the lecture (Braunwald's companion): [1]
| Class | Presentation |
|---|---|
| Rest angina | Angina occurring at rest, prolonged, usually > 20 minutes |
| New-onset angina | New-onset angina of at least CCS class III |
| Crescendo angina | Previously stable angina becoming distinctly more frequent, longer in duration, or lower in threshold (increased by ≥1 CCS class to at least CCS class III) |
High Yield: Acute MI Presentation
Typical Features: [1]
- Middle-age or older men, postmenopausal women
- Severe and prolonged chest pain ( > 30 minutes)
- Associated with nausea, vomiting, diaphoresis, SOB, anxiety
Atypical Features: [1]
- Extrathoracic sites of pain
- GI symptoms alone — heartburn, vomiting
- Profound fatigue, weakness, and anxiety
- Palpitation, dizziness, syncope, stroke or embolism
- Silent — DM, elderly, female, and post-op patients
Why women and the elderly present atypically: Women are more likely to experience fatigue, nausea, and jaw pain rather than classic crushing central chest pain. The elderly often have blunted pain perception and may present with acute confusion or "just not feeling right." Post-operative patients may attribute their symptoms to surgical pain. These atypical presentations lead to diagnostic delay — which is why you must have a high index of suspicion.
The lecture explicitly lists features that should make you think AGAINST myocardial ischaemia: [1]
- Pleuritic pain (sharp/knife-like, worsened by breathing/coughing) → think pericarditis, PE, pneumothorax
- Pain localized to middle/lower abdomen → think GI cause
- Pain localized to tip of one finger (especially over LV apex) → think musculoskeletal/anxiety
- Pain reproduced by movement or palpation of chest wall/arms → think musculoskeletal
- Constant pain persisting for many hours → think musculoskeletal or anxiety (ischaemic pain comes and goes)
- Very brief episodes lasting a few seconds or less → too short for ischaemia
- Pain radiating to lower extremities → not ischaemic
Exam Trap
Students often confuse pleuritic chest pain with ischaemic pain. Ischaemic pain is NEVER sharp, never worsened by breathing, and never reproduced by palpation. If the patient says "it hurts when I press here" or "it's worse when I take a deep breath," think pericarditis, PE, musculoskeletal — not angina.
This table from the lecture (Macleod's) is extremely high yield for exams. Memorise the discriminating features. [1]
| Feature | Angina | MI | Aortic Dissection | Pericardial Pain | Oesophageal Pain |
|---|---|---|---|---|---|
| Site | Retrosternal | Retrosternal | Interscapular/retrosternal | Retrosternal or left-sided | Retrosternal or epigastric |
| Onset | Progressive increase over 1-2 min | Rapid over a few minutes | Very sudden | Gradual; posture may aggravate | Over 1-2 min; can be sudden (spasm) |
| Character | Constricting, heavy | Constricting, heavy | Tearing or ripping | Sharp, stabbing, pleuritic | Gripping, tight, or burning |
| Radiation | Sometimes arms, neck, epigastrium | Often arms, neck, jaw, sometimes epigastrium | Back, between shoulders | Left shoulder or back | Often to back, sometimes arms |
| Associations | Breathlessness | Sweating, nausea, vomiting, SOB, angor animi | Sweating, syncope, neurological signs, limb/mesenteric ischaemia | Flu-like prodrome, SOB, fever | Heartburn, acid reflux |
| Timing | Intermittent, 2-10 min | Acute, prolonged | Acute, prolonged | Acute, variable | Intermittent, often nocturnal |
| Exacerbating/Relieving | Triggered by emotion/exertion/cold; relieved by rest and GTN | Spontaneous; NOT relieved by rest or GTN | Spontaneous; nothing relieves | Sitting up helps; NSAIDs help | Lying flat/foods trigger; nitrates sometimes relieve |
| Severity | Mild to moderate | Usually severe | Very severe | Can be severe | Usually mild; oesophageal spasm can mimic MI |
MCQ from Lecture Slides
MCQ 1 from the lecture: Which feature is most likely associated with myocardial ischaemia-related chest pain?
Answer: Radiation to both arms. [1]
Myocardial ischaemic discomfort is typically substernal with radiation to neck, jaw, shoulder, or arms. Radiation to the back (between shoulder blades) → think aortic dissection. Pain solely below epigastrium or above mandible → rarely angina.
3. Dyspnoea (The Second Cardinal Symptom)
High Yield: Mechanism of Cardiac Dyspnoea
The lecture outlines five mechanisms of dyspnoea in heart disease: [1]
- Increased work of breathing: Left heart failure → ↑ pulmonary capillary wedge pressure ( > 18 mmHg) → oedema of alveolar wall → ↓ lung compliance → ↑ work of breathing
- ↓ Vital capacity: Pulmonary congestion/effusion reduces the lung volume available for gas exchange
- Reflex hyperventilation: Stimulation of juxta-capillary (J) receptors in the alveolar walls by interstitial oedema triggers reflexive rapid breathing
- Bronchial narrowing: Oedematous bronchial walls ("cardiac asthma")
- Hypoxaemia and CO₂ retention: e.g., in cyanotic heart disease
Why left heart failure causes pulmonary oedema (the cascade):
- LV fails → cannot pump blood forward → blood backs up into the left atrium → pressure transmitted to pulmonary veins → pulmonary capillary hydrostatic pressure rises above oncotic pressure → fluid leaks into the interstitium and then alveoli → impaired gas exchange → dyspnoea.
The lecture distinguishes four positional variants: [1]
| Type | Definition | Causes | Mechanism |
|---|---|---|---|
| Orthopnoea | Dyspnoea in the supine position | CHF, COPD, ascites, obesity, anterior mediastinal mass, respiratory muscle weakness | Lying flat → venous return increases → already-failing LV can't handle the extra preload → pulmonary congestion worsens. Also, diaphragm pushed up by abdominal contents |
| Trepopnoea | Dyspnoea in the lateral position | Unilateral lung disease, effusion, airway obstruction | Lying on the diseased side impairs ventilation of the dependent lung |
| Platypnoea | Dyspnoea in the upright position (opposite of orthopnoea) | Intracardiac shunt, parenchymal lung shunt, hepatopulmonary shunt | Standing increases shunt through patent foramen ovale or intrapulmonary shunts (gravity-dependent) |
| Paroxysmal Nocturnal Dyspnoea (PND) | Sudden awakening from sleep with severe breathlessness | CHF | During sleep, gradual reabsorption of dependent oedema fluid increases intravascular volume → pulmonary congestion → awakens patient gasping |
High Yield: Orthopnoea vs PND for Heart Failure
Orthopnoea is sensitive but non-specific for heart failure. [1]
PND is non-sensitive but specific for heart failure. [1]
This means: Many patients with HF have orthopnoea, but orthopnoea can also occur in COPD, obesity, etc. In contrast, PND is uncommon, but when present, it is a very strong indicator that symptoms are due to HF.
MCQ from Lecture Slides
MCQ 2 from the lecture: Which symptom is most suggestive of heart failure?
Answer: Paroxysmal nocturnal dyspnoea. [1]
PND is a very strong indicator that symptoms are due to HF, particularly when other conditions that result in nocturnal awakening (postnasal drip, oesophageal reflux, orthopaedic issues) are excluded.
The lecture highlights specific associated symptoms that help differentiate causes: [1]
| Associated Symptom | What It Suggests | Mechanism |
|---|---|---|
| Dry, unproductive cough | Pulmonary congestion in HF, or ACE inhibitor side effect | Congestion irritates bronchial mucosa; ACEi → ↑ bradykinin → cough reflex |
| Haemoptysis (bright red) | Rupture of submucosal pulmonary venules in mitral stenosis or HF | Elevated pulmonary venous pressure → fragile submucosal veins rupture |
| Haemoptysis (dark blood/clots) | Pulmonary embolism | Pulmonary infarction → necrotic tissue bleeds |
| Pink, frothy sputum | Acute pulmonary oedema | Fluid floods alveoli; mixed with air = frothy; blood-tinged = pink |
| Wheezing | "Cardiac asthma" — HF causing bronchial oedema | Oedematous bronchial walls narrow airways, mimicking asthma |
This table from the lecture is a common exam question: [1]
| Feature | Cardiac | Respiratory |
|---|---|---|
| Duration | Short (months) | Long (years) |
| PND | Characteristic | Nil |
| Orthopnoea | Characteristic | Maybe present (COPD/obesity) |
| Oedema | Often present | Present in cor pulmonale only |
| Associated symptoms | Angina, palpitation | Cough, sputum, wheezing |
| Physical examination | Oedema, ↑JVP, cardiomegaly, basal crepitations, tachycardia | Inflated chest, wheezing |
Why cardiac dyspnoea has shorter duration: Heart failure can develop relatively quickly (e.g., after MI, acute valve dysfunction), whereas COPD/ILD develop over decades of exposure. However, chronic HF can also present over years, so this is a general guide, not absolute.
This is the standard grading system for heart failure symptom severity: [1]
| Class | Description |
|---|---|
| I | No limitations. Ordinary physical activity does not cause undue fatigue, dyspnoea, or palpitation (asymptomatic LV dysfunction) |
| II | Slight limitation. Comfortable at rest. Ordinary physical activity → fatigue, palpitation, dyspnoea, or angina ("mild" HF) |
| III | Marked limitation. Less than ordinary activity leads to symptoms ("moderate" HF) |
| IV | Symptoms at rest. Any physical activity increases discomfort ("severe" HF) |
Why NYHA matters: It determines treatment intensity, prognostication, and eligibility for device therapy (e.g., CRT, ICD). It's also a mandatory part of any HF case presentation. [2]
4. Palpitation (The Third Cardinal Symptom)
Palpitation: the feeling that heart action is more vigorous than usual, or its perception is unpleasant — described as "pounding," "stopping," "jumping," or "racing" in the chest. [1]
Key history points: [1]
- Physiological (sinus tachycardia) vs pathological
- Character: missed beat, irregular, or sustained
- Trigger: coffee, tea, exercise, postural change, meal, emotion
- Onset and offset: Sudden onset/offset → SVT or VT; Gradual → sinus tachycardia
- Haemodynamic effects: dizziness, presyncope, syncope
- Duration, frequency, pattern
- Associated symptoms: syncope and chest pain
- Rate and rhythm: Ask the patient to tap out the rate and rhythm of the episode [1]
This table from the lecture maps historical features to likely arrhythmias: [1]
| Historical Feature | Possible Cause |
|---|---|
| Rapid fluttering | ST, SVT, AF, AFL, VT |
| Flip-flopping | PVCs and PACs |
| Intermittent forceful beats | PVCs |
| Irregular pounding in neck | AV dissociation: PVCs, VT, CHB |
| Regular pounding in neck ("frog sign") | SVT (cannon A waves) |
| Young age of onset | SVT |
| Sudden onset | AVNRT, AVRT, VT |
| Gradual onset | AT, sinus tachycardia |
| Response to vagal manoeuvres | AVNRT, AVRT |
| Syncope | VT, SVT, CHB |
| Occurs at night in bed | PACs, PVCs, AF |
| Occurs during exercise | SVT, AF, VT (structurally normal heart) |
Why "frog sign" matters: In SVT (especially AVNRT), the atria and ventricles contract simultaneously → the atria contract against closed AV valves → blood refluxes into the jugular veins → visible regular pounding in the neck.
Why sudden onset/offset is important: Sinus tachycardia gradually accelerates ("warm-up") and decelerates. In contrast, re-entrant tachycardias (AVNRT, AVRT) start and stop abruptly because the re-entrant circuit either fires or doesn't — there's no gradual transition.
From the lecture: [1]
| Feature | Extrasystoles | Sinus Tachycardia | SVT | AF | VT |
|---|---|---|---|---|---|
| Onset | Sudden | Gradual | Sudden, with "jump" | Sudden | Sudden |
| Character | "Jump", missed beat | Regular, fast, pounding | Regular, fast | Irregular, usually fast | Regular, fast |
| Associations | Nil | Anxiety | Polyuria, lightheadedness | Polyuria, breathlessness | Presyncope, syncope |
| Timing | Brief | A few minutes | Minutes to hours | Variable | Variable |
| Triggers | Fatigue, caffeine, alcohol | Exercise/anxiety | Usually at rest; bending | Exercise/alcohol; often spontaneous | Exercise; often spontaneous |
| Relieving | Walking (increases sinus rate, suppresses ectopics) | — | Vagal manoeuvres may relieve | — | — |
| Severity | Mild (usually) | Mild-moderate | Moderate-severe | Very variable | Often severe |
Why SVT causes polyuria: Atrial stretch during SVT releases atrial natriuretic peptide (ANP), which promotes natriuresis and diuresis. Patients often notice they need to urinate frequently during or after an episode.
MCQ from Lecture Slides
MCQ 3 from the lecture: Which feature is suggestive of pathologic palpitation due to cardiac arrhythmias?
Answer: Associated with syncope. [1]
Gradual onset with warm-up/cool-down → sinus tachycardia. Associated with anxiety → physiological stress. Associated with syncope → haemodynamically significant arrhythmia.
5. Syncope (The Fourth Cardinal Symptom)
Cardiac Syncope: Transient loss of consciousness due to inadequate cerebral blood flow with spontaneous recovery. [1]
From the lecture: [1]
| Cause | Mechanism |
|---|---|
| Neurocardiogenic (vasovagal) syncope | Excessive vagal tone → bradycardia and vasodilation → ↓ BP → ↓ cerebral perfusion |
| Arrhythmia | SVT, VT, Adams-Stokes attack (asystole or ventricular arrhythmia in heart block) |
| Exertional syncope | Severe aortic stenosis, HOCM, CAD → fixed cardiac output that can't increase with exertion → ↓ cerebral perfusion |
| Carotid sinus syncope | Reflex bradycardia or hypotension from hypersensitive carotid sinus baroreceptors |
| Postural syncope | Orthostatic hypotension (autonomic dysfunction, hypovolaemia, medications) |
High Yield: Exertional Syncope
Exertional syncope is a RED FLAG for severe aortic stenosis or HOCM. In AS, the fixed outflow obstruction prevents the heart from increasing cardiac output during exercise. In HOCM, dynamic LVOT obstruction worsens during exercise (increased contractility, decreased preload from sweating). Both can cause sudden death. Any patient with exertional syncope needs urgent cardiology assessment. [1]
The lecture emphasises asking about:
- Provoking factors: pain, micturition, exercise, defecation, stress, standing → vasovagal; exertion → structural heart disease
- Warning symptoms: sweating, nausea → vasovagal; palpitations → arrhythmia; none → arrhythmia or structural
- Duration of LOC
- Recovery: rapid and complete → syncope; slow with confusion → seizure
- Witness account: what did bystanders see? Seizure activity can occur in syncope (convulsive syncope) secondary to cerebral hypoperfusion — this is NOT epilepsy [1]
This differentiation table is very high yield: [1]
| Clinical Feature | Syncope | Seizures |
|---|---|---|
| LOC precipitated by pain, micturition, exercise, stress | + | – |
| Sweating and nausea before/during | + | – |
| Aura | – | + |
| Tongue biting | – | + |
| Disorientation after the event | – | + |
| Clonic/myoclonic jerks | +/– (can occur in syncope!) | ++ |
| Slowness in returning to consciousness | – | + |
| Unconscious > 5 minutes | – | + |
Why syncope can cause jerks: When cerebral blood flow drops critically, the brainstem release phenomena can produce brief myoclonic jerks. These are usually < 15 seconds and not rhythmic. In contrast, epileptic seizures produce sustained, rhythmic, tonic-clonic movements lasting longer. The key discriminator is the post-event state: syncope patients recover quickly and are oriented; seizure patients have a prolonged post-ictal period with confusion.
From the lecture's cardiac symptoms table: [1]
Cardiovascular causes of oedema: Heart failure, constrictive pericarditis, venous stasis, lymphoedema
Other causes: Nephrotic syndrome, liver disease, drugs (NSAIDs, CCBs like amlodipine, glucocorticoids), immobility
Why right heart failure causes peripheral oedema: RV failure → blood backs up into systemic venous circulation → ↑ venous hydrostatic pressure → fluid leaks into interstitial space in gravity-dependent areas (ankles when standing, sacrum when lying).
Cardiac vs Renal oedema clue (from supporting notes): [3]
- HF patients have orthopnoea → sleep propped up → fluid doesn't accumulate in face → no periorbital oedema
- Renal patients can lie flat → fluid redistributes overnight → periorbital oedema present in the morning
8. Comprehensive Cardiac History: Beyond Symptoms
Key PMH items for cardiac patients: [1]
- Previous angina, MI, bypass grafts, stents, valve replacements
- Atrial fibrillation
- Stroke or TIA
- Peripheral vascular disease
- Hypertension, hyperlipidaemia (CV risk factors)
- Rheumatic fever (→ valvular disease)
- Dental work (→ risk of infective endocarditis)
- Prior tests and interventions (catheterisation, echo results)
- TB (pericarditis)
- Hyperthyroidism (AF, high-output HF)
- Hospital admissions — when and why?
Cardiovascular medications to specifically ask about: [1]
Beta-blockers, calcium channel blockers, ACE inhibitors, diuretics, statins, antiplatelets, anticoagulants, GTN spray
Also ask about: [1]
- Contraceptive pill → increased risk of thromboembolic disease
- Over-the-counter drugs → NSAIDs/aspirin
- Herbal remedies → e.g., St John's Wort (enzyme inducer → affects warfarin levels)
- Allergies
Drug-Symptom Interaction Table (Macleod's, from lecture): [1]
| Symptom | Medication That Can Cause/Worsen It |
|---|---|
| Angina | Thyroxine, drug-induced anaemia (aspirin, NSAIDs) |
| Dyspnoea | Beta-blockers (in asthmatics), CCBs (verapamil, diltiazem), NSAIDs → exacerbate HF |
| Palpitation | Thyroxine, β2 agonists (salbutamol), digoxin toxicity, hypokalaemia from diuretics, tricyclics |
| Syncope/presyncope | Vasodilators (nitrates, alpha-blockers, ACEi, ARBs), rate-limiting agents (beta-blockers, verapamil, diltiazem, digoxin, amiodarone) |
| Oedema | Glucocorticoids, NSAIDs, CCBs (nifedipine, amlodipine) |
Exam Point: Why Not on Standard Treatment?
If a patient with known CVD is NOT taking recognized standard treatment, the reason should be established. Example from the lecture: Why no statin in a patient with previous MI? — "Because it caused muscle pains" (statin-induced myopathy). [1]
Specifically ask about: [1]
- Cardiovascular disease at a young age (MI, hypertension, thrombophilia)
- Are parents still in good health? If deceased → age and cause of death
- Any unexplained deaths in young relatives? → long QT syndrome / channelopathies [1]
Why this is critical: Inherited cardiac conditions (familial hypercholesterolaemia, HOCM, long QT, Brugada) can cause sudden cardiac death in young people. A family history of sudden death mandates screening. [7]
From the lecture: [1]
| Factor | Specific Questions | Why It Matters |
|---|---|---|
| Smoking | Cigarettes/day × years = pack-years | Strongest modifiable CVD risk factor |
| Alcohol | Units/week, type, volume, strength | Excess → alcoholic cardiomyopathy, AF ("holiday heart"), hypertension |
| Recreational drugs | Especially cocaine | Coronary artery vasospasm → MI even in young patients |
| Diet | Overweight? Fatty foods? Salt intake? | CV risk factors |
| Exercise | Baseline activity level | Determines functional capacity and management goals |
| Living situation | House/bungalow? Stairs? Who lives with them? Carer input? | Important for discharge planning after cardiac events |
| ADLs | Independent? Self-hygiene? Shopping? | Assesses functional impact of disease |
| Occupation | Sedentary? (e.g., taxi driver → ↑ CV risk) | Also important for driving restrictions post-MI, post-device |
Pregnancy, delivery, menopause [1]
Why: Pre-eclampsia is a risk factor for future hypertension and CVD. Peripartum cardiomyopathy. Menopause removes the cardioprotective effect of oestrogen → CVD risk increases post-menopause.
This may pick up symptoms the patient failed to mention: [1]
- Respiratory: Dyspnoea, cough, sputum, wheeze, haemoptysis, chest pain
- GI: Appetite, nausea, vomiting, indigestion, dysphagia, weight loss, abdominal pain, bowel habit
- Urinary: Volume, frequency, dysuria, urgency, incontinence
- CNS: Vision, headache, motor/sensory disturbance, LOC, confusion
- MSK: Bone/joint pain, muscular pain
- Dermatology: Rashes, skin breaks, ulcers, lesions
This comprehensive table from the lecture (Macleod's) maps each symptom to cardiovascular and non-cardiovascular causes: [1]
| Symptom | Cardiovascular Causes | Other Causes |
|---|---|---|
| Chest discomfort | MI, Angina, Pericarditis, Aortic dissection | Oesophageal spasm, Pneumothorax, MSK pain |
| Breathlessness | Heart failure, Valvular disease, Angina, PE, Pulmonary HTN | Respiratory disease, Anaemia, Obesity, Anxiety |
| Palpitation | Tachyarrhythmias, Ectopic beats | Anxiety, Hyperthyroidism, Drugs |
| Syncope/presyncope | Arrhythmias, Postural hypotension, Aortic stenosis, HOCM, Atrial myxoma | Simple faints, Epilepsy, Anxiety |
| Oedema | Heart failure, Constrictive pericarditis, Venous stasis, Lymphoedema | Nephrotic syndrome, Liver disease, Drugs, Immobility |
10. Integration with Related Material
Key learning point: CXR findings in left heart failure correlate with left atrial pressure — upper lobe diversion at 10-15 mmHg, Kerley B lines at 15-20 mmHg, and alveolar oedema above 25 mmHg. [8] This correlates with the lecture's mechanism of dyspnoea where PCWP > 18 mmHg causes interstitial oedema. [1]
Heart failure is a clinical diagnosis using the Framingham Criteria: requires ≥2 major criteria OR 1 major + 2 minor criteria. Major criteria include PND, orthopnoea, JVP elevation, S3 gallop, cardiomegaly, pulmonary oedema on CXR. [2]
When taking history for a hypertensive patient, also assess for target organ damage: brain (headache, TIA), eyes (visual impairment), heart (chest pain, palpitations, SOB), kidneys (polyuria, nocturia), and peripheral arteries (claudication). [4]
High Yield Summary
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Structure
- PC → HPC (SOCRATES) → Cardiac symptoms (chest pain, dyspnoea, palpitations, syncope, oedema, claudication, systemic) → PMH → Risk factors (smoking, HT, DM, hyperlipidaemia, FHx) → DHx → FHx → SHx → Systemic Enquiry
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Chest Pain
- Ischaemic pain = retrosternal, constricting, radiates to arm/jaw, 2-10 min, triggered by 4 "E"s, relieved by rest/GTN.
- Atypical = sharp, positional, pleuritic, localized to fingertip, constant for hours. 25% of ischaemia is silent (DM, elderly).
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Dyspnoea
- PND is specific for HF; orthopnoea is sensitive but not specific. Mechanism: LHF → ↑PCWP → alveolar oedema → ↓compliance → ↑work of breathing.
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Palpitation
- Ask to tap rhythm. Sudden onset → re-entrant (SVT/VT). Gradual → sinus tachycardia. Syncope with palpitations → haemodynamically significant arrhythmia.
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Syncope
- Exertional = red flag for AS/HOCM. Differentiate from seizure: syncope has prodromal nausea/sweating, rapid recovery, no tongue biting, no post-ictal confusion.
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Grading
- CCS I-IV for angina; NYHA I-IV for heart failure.
Active Recall - Cardiovascular History Taking
[1] Lecture slides: CFB (MED05) Cardiovascular (I) Physical Examination (History Taking).pdf (all pages) [2] Senior notes: Block A - Shortness of breath on exertion_ heart failure.pdf (Framingham Criteria, NYHA classification) [3] Senior notes: Block A - Glomerular and Tubulo-interstitial Diseases and Acute Kidney Injury.pdf (cardiac vs renal oedema differentiation) [4] Senior notes: Block A - High blood pressure_ hypertension.pdf (target organ damage history) [5] Lecture slides: Clinical Demonstration_Vascular.pdf (peripheral vascular history) [6] Senior notes: Block A - Chest Pain - Department of Medicine.pdf (premature CVD definition: male < 55, female < 65) [7] Senior notes: Introduction to Clinical pharmacology (I) (Pharmaco- Genomics, Precision Medicine).pdf (familial hypercholesterolaemia) [8] Senior notes: learning_points_output.txt (Three Cases of Dyspnoea learning points)
CFB PSY01 An Introduction To Psychiatry
An introductory overview of psychiatry covering its scope, the biopsychosocial model of mental illness, psychiatric history-taking, mental status examination, and classification systems used in diagnosing mental disorders.
CFB MED06 Cardiovascular (II) Physical Examination
Systematic clinical assessment of the heart and vasculature through inspection, palpation, percussion, and auscultation to evaluate cardiac structure, function, and hemodynamic status.