Cardiology Investigations

• Start here: Choosing the Right Test
• Bedside and simple tests: Key Bedside Signs | Measuring Blood Pressure | Chest X-ray in Heart Disease
• The ECG: Reading an ECG | Cardiac Axis | Conduction Problems | Hypertrophy and Chamber Enlargement | Ischaemia and Infarction | Other Important ECG Patterns | Normal Variants and the Athlete's ECG
• Rhythm monitoring and testing: Ambulatory Rhythm Monitoring | Exercise Testing | Tilt Testing and EP Studies
• Imaging: Echocardiography | CT Coronary Angiography | Functional (Stress) Imaging | Cardiac MRI | Nuclear Cardiology and PET | Invasive Coronary Angiography | Right Heart Catheterisation | Safety of Cardiac Tests
• Blood tests: Troponin | Natriuretic Peptides | Other Cardiac Blood Tests
• Revision: Tests at a Glance | ECG Patterns at a Glance | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🔬 Cardiac investigations answer three questions: what is the rhythm, how is the heart structured and working, and is the blood supply adequate? This chapter starts with which test to choose for each common presentation, then explains how to read an ECG systematically, when to use each imaging test (echo, CT, MRI, nuclear, angiography), how to interpret troponin and natriuretic peptides, and how to keep patients safe during tests.
Your four questions for every patient: What does the ECG show, and has it changed? What is the structure and function on echo? Is there coronary disease, and is it causing ischaemia? Do the blood tests fit the clinical picture?

Choosing the Right Test

Start with the question you need answered. Every patient with a suspected heart problem needs a 12-lead ECG; most also need basic bloods (FBC, U&E, TFTs, HbA1c, lipids).

• Syncope red flags — refer for specialist assessment within 24 hours (NICE CG109):
  • Abnormal ECG (e.g. heart block, long QT, Brugada, WPW, LVH, pathological Q waves).
  • Heart failure, or a new murmur.
  • Collapse during exertion.
  • Family history of sudden cardiac death under 40, or an inherited heart condition.
  • New or unexplained breathlessness.
  • Age over 65 with syncope and no warning symptoms.

💡 Clinical Pearl: Before ordering a test, ask: "What will I do differently with the result?" The best test is the one that answers the clinical question with the least risk — often the cheapest (ECG, echo) comes first.

Key Bedside Signs

Pulse character:

• Slow-rising, low-volume — aortic stenosis.
• Collapsing (water-hammer) — aortic regurgitation, PDA, high-output states.
• Bisferiens (double peak) — mixed aortic valve disease, HCM.
• Pulsus alternans (alternating strong and weak beats) — severe LV failure.
• Pulsus paradoxus (systolic fall of more than 10 mmHg on inspiration) — tamponade, severe asthma.
• Irregularly irregular — AF.
• Radio-femoral delay — coarctation.

Jugular venous pressure (JVP):

• Raised — right heart failure, fluid overload, tamponade, constriction, SVC obstruction (non-pulsatile).
• Large V waves — tricuspid regurgitation.
• Cannon A waves — complete heart block, VT (atria contract against closed valves).
• Absent A waves — AF.
• Kussmaul's sign (JVP rises on inspiration) — constrictive pericarditis, restrictive cardiomyopathy, RV infarction.

Heart sounds:

• Loud S1 — mitral stenosis.
• Soft S2 — severe aortic stenosis.
• Loud P2 — pulmonary hypertension.
• Fixed split S2 — ASD.
• S3 — heart failure (or normal in young people).
• S4 — stiff ventricle (LVH, HCM).
• Opening snap — mitral stenosis.
• Ejection click — bicuspid aortic valve.
• Mid-systolic click — mitral valve prolapse.
• Pericardial knock — constriction.

Murmurs are covered in detail in the Valvular Heart Disease chapter.

Measuring Blood Pressure

• Technique:
  • Seated and relaxed for 5 minutes; arm supported at heart level; correct cuff size (too small a cuff over-reads).
  • Measure both arms at the first visit — a difference of more than 15 mmHg on repeat is abnormal (subclavian stenosis, coarctation, dissection); use the higher arm from then on.
  • If the first reading is 140/90 or more, take a second (and third if the first two differ); record the lower of the last two.
  • Irregular pulse (e.g. AF) — use a manual (auscultatory) measurement; automated devices can be inaccurate.
• Confirming hypertension (NICE NG136):
  • Clinic BP 140/90 to 179/119 — offer ambulatory BP monitoring (ABPM), or home monitoring if ABPM is unsuitable.
  • Stage 1 — ABPM daytime average (or home average) 135/85 or more.
  • Stage 2 — ABPM or home average 150/95 or more.
  • Home monitoring — two readings a minute apart, morning and evening, for at least 4 days (ideally 7); discard the first day and average the rest.
  • Clinic BP 180/120 or more — look for target organ damage; same-day referral if there is retinal haemorrhage or papilloedema (accelerated hypertension), or life-threatening symptoms (chest pain, confusion, heart failure, AKI).
• White-coat hypertension — high in clinic, normal at home (about 20 mmHg difference). Masked hypertension — normal in clinic, high at home (higher risk than it looks).
• Lying and standing BP — lie the patient down for 5 minutes, then measure after 1 and 3 minutes of standing.
  • Orthostatic hypotension — a fall of 20 mmHg or more systolic or 10 mmHg or more diastolic (or systolic below 90 mmHg) within 3 minutes, often with symptoms.
  • Causes — drugs (antihypertensives, diuretics, alpha-blockers, nitrates, antidepressants, levodopa), dehydration, autonomic failure (Parkinson's disease, diabetes, multiple system atrophy), prolonged bed rest.
  • A large heart rate rise (30 or more) without BP fall suggests PoTS.
• Tests at diagnosis of hypertension — urine albumin:creatinine ratio, urine dipstick for blood, U&E and eGFR, HbA1c, lipids, 12-lead ECG, fundoscopy; consider secondary causes (renin and aldosterone, metanephrines) in young people or resistant hypertension (see the Hypertension chapter).

Chest X-ray in Heart Disease

• Heart size — cardiothoracic ratio over 0.5 on a PA film suggests cardiomegaly. AP (portable) and supine films exaggerate heart size, so don't rely on them.
• Heart failure — remember ABCDE:
  • Alveolar oedema ("bat's wing" shadowing around the hila).
  • B — Kerley B lines (short horizontal lines at the lung edges — interstitial oedema).
  • Cardiomegaly.
  • Dilated upper lobe vessels (upper lobe diversion).
  • Effusions (pleural), and fluid in the fissures.
• Large pericardial effusion — enlarged, globular ("water bottle") heart with clear lungs; confirm with echo.
• Left atrial enlargement (mitral stenosis) — double right heart border, straightened left heart border, splayed carina.
• Calcification — valves (aortic, mitral annulus), pericardium (constrictive pericarditis), LV aneurysm, aortic knuckle.
• Pulmonary hypertension — enlarged central pulmonary arteries with "pruned" peripheral vessels.
• Aorta — widened mediastinum in aortic dissection or aneurysm (but the X-ray is normal in many dissections — use CT).
• Congenital heart disease:
  • Boot-shaped heart — tetralogy of Fallot.
  • "Egg on a string" — transposition of the great arteries.
  • Rib notching and a "figure of 3" sign — coarctation of the aorta.
  • Plethoric lungs — left-to-right shunts (ASD, VSD, PDA).
• Devices and surgery — sternal wires (previous surgery), prosthetic valves, pacemaker or ICD leads (check position and look for lead fracture or pneumothorax after implantation), LAA occluders.
• Other causes of breathlessness — pneumonia, pneumothorax, effusion, lung cancer, interstitial lung disease.

Reading an ECG

Paper and timing (standard speed 25 mm/s):

• 1 small square = 0.04 s; 1 large square = 0.2 s.
• Heart rate = 300 ÷ number of large squares between R waves (regular rhythm), or the number of QRS complexes on a 10-second strip × 6.

A systematic approach — every time:

• 1. Patient details, date, calibration (10 mm = 1 mV).
• 2. Rate.
• 3. Rhythm — regular or irregular? P wave before every QRS? (sinus rhythm).
• 4. Axis.
• 5. P waves — shape (P mitrale, P pulmonale), absent (AF), flutter waves.
• 6. PR interval — normal 0.12–0.20 s:
  • Long — heart block.
  • Short — pre-excitation (WPW).
• 7. QRS — width (normal below 0.12 s), height (hypertrophy or low voltage), Q waves, delta waves.
• 8. ST segment — elevation or depression.
• 9. T waves — inversion, peaked, flattened.
• 10. QT interval — corrected for rate (QTc).
  • Normal below about 440 ms (men) and 460 ms (women).
  • Above 500 ms — high risk of torsades.
• 11. Compare with old ECGs — the most useful step of all.

💡 Clinical Pearl: Always compare with a previous ECG. A "new" LBBB, Q wave or T wave inversion is far more meaningful than one that has been there for years.

Cardiac Axis

• What it shows: The overall direction of electrical activity through the ventricles. Normal is −30° to +90°.
• Quick method — look at the QRS in leads I and II (or aVF):
  • Both positive — normal axis.
  • Lead I positive, lead II negative — left axis deviation.
  • Lead I negative, aVF positive — right axis deviation.
• Causes of left axis deviation:
  • Left anterior fascicular block (the commonest).
  • Inferior MI.
  • LVH.
  • WPW.
  • Primum ASD.
  • Hyperkalaemia.
• Causes of right axis deviation:
  • RV hypertrophy or strain — pulmonary hypertension, PE, COPD.
  • Left posterior fascicular block.
  • Lateral MI.
  • Dextrocardia.
  • Secundum ASD.
  • Normal in tall, thin young people.

Conduction Problems

• First-degree AV block: PR above 0.20 s; every P conducted. Usually benign.
• Second-degree AV block:
  • Mobitz I (Wenckebach) — PR lengthens until a beat is dropped. Usually AV node, often benign.
  • Mobitz II — sudden dropped beats with a constant PR. Below the AV node — risk of complete block, needs a pacemaker.
  • 2:1 block — cannot classify as type I or II.
• Third-degree (complete) heart block: P waves and QRS complexes are independent (AV dissociation). Slow escape rhythm; broad complexes mean a lower, less reliable escape.
• Right bundle branch block (RBBB):
  • QRS 0.12 s or more, RSR′ in V1 ("M"), wide slurred S in I and V6.
  • Can be normal, or seen with ASD, PE or RV strain.
• Left bundle branch block (LBBB):
  • QRS 0.12 s or more, broad notched R in I, aVL and V6 ("M" in V6), deep S in V1 ("W").
  • Always abnormal — IHD, hypertension, cardiomyopathy, aortic stenosis.
  • New LBBB with chest pain may be an MI.
• Fascicular blocks:
  • Left anterior fascicular block — left axis deviation.
  • Left posterior fascicular block — right axis deviation.
  • Bifascicular block — RBBB plus a fascicular block.
  • Trifascicular — bifascicular plus a long PR. With syncope, this suggests intermittent complete heart block.
• Pre-excitation (WPW): Short PR, delta wave (slurred QRS upstroke), broad QRS — an accessory pathway.

Hypertrophy and Chamber Enlargement

• Left ventricular hypertrophy:
  • Sokolow–Lyon criterion: S wave in V1 plus R wave in V5 or V6 above 35 mm.
  • Often with a "strain" pattern — ST depression and T wave inversion in lateral leads.
  • Causes: Hypertension, aortic stenosis, HCM, coarctation.
  • Voltage criteria alone are common (and normal) in young, thin people and athletes.
• Right ventricular hypertrophy:
  • Dominant R wave in V1; right axis deviation; T wave inversion in V1–V3; deep S waves in V5–V6.
  • Causes: Pulmonary hypertension, pulmonary stenosis, COPD, congenital heart disease.
• Causes of a dominant R wave in V1:
  • RVH.
  • Posterior MI.
  • RBBB.
  • WPW (type A).
  • Dextrocardia.
  • HCM.
  • Normal in children.
• Atrial enlargement:
  • P mitrale — broad, notched P in II, suggesting left atrial enlargement (mitral stenosis).
  • P pulmonale — tall, peaked P in II, suggesting right atrial enlargement (pulmonary hypertension).
• Low-voltage QRS (small complexes in all leads):
  • Pericardial effusion.
  • Obesity; emphysema.
  • Hypothyroidism.
  • Cardiac amyloidosis — low voltages with a thick heart on echo is a classic clue.

Ischaemia and Infarction

• ST elevation in 2 or more contiguous leads — acute coronary occlusion (STEMI). See the Cardiac Emergencies chapter for criteria and equivalents.
• ST depression and T wave inversion — ischaemia (NSTEMI, unstable angina), strain, digoxin, or reciprocal change.
• Pathological Q waves — previous transmural MI (wider than 0.04 s, or deeper than 25% of the R wave).
• Wellens' sign: Deep or biphasic T wave inversion in V2–V3 in a pain-free patient after chest pain — critical proximal LAD stenosis. Needs urgent angiography, and no exercise testing.
• Persistent ST elevation weeks after an MI — LV aneurysm.

Coronary territories:

Other Important ECG Patterns

• Hyperkalaemia: Peaked T waves, then flat P waves, long PR, broad QRS, sine wave, VF.
• Hypokalaemia: Flat T waves, ST depression, U waves, apparent long QT.
• Hypocalcaemia: Long QT. Hypercalcaemia: Short QT.
• Hypomagnesaemia: Long QT, torsades.
• Digoxin effect: "Reverse tick" (sloping) ST depression — not by itself toxicity. Toxicity causes almost any arrhythmia.
• Hypothermia: Bradycardia, J (Osborn) waves, long intervals, shivering artefact.
• Pericarditis: Widespread saddle ST elevation with PR depression.
• Pulmonary embolism:
  • Sinus tachycardia — the commonest finding.
  • RV strain (T inversion V1–V4), RBBB, right axis deviation.
  • S1Q3T3 (uncommon).
• Long QT: Congenital, or acquired (drugs, low potassium, low magnesium, low calcium, bradycardia).
• Brugada pattern: Coved ST elevation in V1–V2 with RBBB-like appearance — risk of sudden death. Unmasked by fever and some drugs.
• ARVC: Epsilon waves and T wave inversion in V1–V3.
• HCM: Marked LVH, deep narrow Q waves, giant T wave inversion (apical HCM).
• Raised intracranial pressure or subarachnoid haemorrhage: Deep, wide T wave inversion ("cerebral T waves"), long QT.
• Dextrocardia: Inverted P and QRS in lead I; poor R wave progression; reversed limb leads look similar (check lead placement).

Normal Variants and the Athlete's ECG

Common, normal findings — especially in trained athletes:

• Sinus bradycardia (even 30–40 at rest); sinus arrhythmia (rate varies with breathing).
• First-degree AV block and Mobitz I (Wenckebach) at night.
• Isolated voltage criteria for LVH.
• Early repolarisation — ST elevation with J point notching in the lateral and inferior leads.
• T wave inversion in V1–V4 preceded by J point elevation — normal in Black athletes.
• Incomplete RBBB.
• T wave inversion in V1–V3 in children and adolescents (under 16).

Abnormal findings that need investigation (international athlete ECG criteria):

• T wave inversion in the lateral or inferolateral leads (HCM, cardiomyopathy).
• ST depression.
• Pathological Q waves.
• LBBB.
• Pre-excitation.
• Long QT (QTc 470 ms or more in men, 480 ms or more in women).
• Brugada pattern; epsilon waves.
• Mobitz II or complete heart block.
• Frequent ventricular ectopics; atrial or ventricular arrhythmias.

Ambulatory Rhythm Monitoring

Choose the monitor to match how often symptoms happen:

• Daily symptoms: 24–48-hour Holter monitor.
• Weekly symptoms: Patch monitors (up to 14 days) or 7-day recorders.
• Less frequent symptoms: Event recorders — patient-activated or looping, worn for weeks.
• Rare symptoms (e.g. unexplained syncope every few months): Implantable loop recorder — a small device under the skin that records for up to 3 years. Also used to look for AF after cryptogenic stroke.
• Consumer devices (smartwatches, handheld ECG devices): Can capture AF and other arrhythmias during symptoms. A clinician should confirm the diagnosis from a recorded ECG trace.

What counts: A symptom with a normal rhythm is as useful as one with an arrhythmia — it rules out an arrhythmic cause.

Exercise Testing

• Exercise ECG (treadmill):
  • No longer recommended for diagnosing coronary disease (NICE CG95) — sensitivity and specificity are poor.
  • Still useful for:
    • Exercise-related symptoms and arrhythmias (e.g. CPVT, exercise-induced AF).
    • Heart rate response (chronotropic incompetence).
    • BP response.
    • Assessing exercise capacity and prognosis.
    • Asymptomatic severe aortic stenosis (specialist).
    • Testing an accessory pathway in WPW.
  • Contraindications:
    • Acute MI or ACS.
    • Symptomatic severe aortic stenosis.
    • Uncontrolled arrhythmia or heart failure.
    • Acute myocarditis or pericarditis.
    • Aortic dissection.
    • Wellens' pattern.
• Cardiopulmonary exercise testing (CPET): Measures oxygen uptake. Separates heart, lung and fitness causes of breathlessness; assesses heart failure severity (transplant assessment) and fitness for major surgery.

Tilt Testing and EP Studies

• Head-up tilt table test:
  • The patient is tilted to about 70° for up to 45 minutes, with continuous BP and heart rate monitoring.
  • Reproduces vasovagal syncope, shows delayed orthostatic hypotension, and diagnoses postural orthostatic tachycardia syndrome (PoTS) — a heart rate rise of 30 or more without hypotension.
• Carotid sinus massage (with monitoring, in people over 40 with unexplained syncope; avoid with carotid disease or recent stroke): A pause of more than 3 seconds or a large BP fall suggests carotid sinus hypersensitivity.
• Electrophysiology (EP) study:
  • Catheters inside the heart record electrical activity and try to trigger arrhythmias.
  • Used to diagnose SVT mechanisms, assess conduction disease, and risk-stratify some patients.
  • Usually combined with catheter ablation.

Echocardiography

• Transthoracic echo (TTE) — the workhorse of cardiology. It shows:
  • LV size and function (ejection fraction; regional wall motion).
  • Valves — stenosis, regurgitation, vegetations.
  • Wall thickness (hypertrophy, HCM, amyloid).
  • Diastolic function and filling pressures.
  • Atrial size.
  • RV function and estimated pulmonary artery pressure.
  • Pericardial effusion.
  • Congenital defects; intracardiac masses and thrombus.
• Transoesophageal echo (TOE) — a probe in the oesophagus, under sedation. Much clearer views of the back of the heart:
  • Endocarditis (prosthetic valves, abscesses).
  • Left atrial appendage thrombus before cardioversion.
  • Mitral valve assessment before repair.
  • ASD and PFO.
  • Aortic dissection.
  • Guiding structural procedures.
• Stress echo (exercise or dobutamine):
  • Shows ischaemia as walls that stop moving well under stress.
  • Assesses viability and low-flow aortic stenosis.
• Bubble contrast echo: Agitated saline injected into a vein to look for shunts — PFO (after cryptogenic stroke) and pulmonary AVMs.
• Contrast echo: Improves image quality when windows are poor; detects LV thrombus.
• Global longitudinal strain: Detects early heart muscle damage — e.g. during chemotherapy (cardio-oncology).

CT Coronary Angiography

• NICE CG95: CT coronary angiography (CTCA) is the first-line test for people with stable chest pain that could be angina — typical or atypical angina, or non-anginal pain with an abnormal resting ECG. Clinical assessment alone can diagnose angina in some people.
• What it shows:
  • Coronary anatomy and plaques.
  • The degree of narrowing.
  • High-risk plaque features.
  • Coronary anomalies.
  • Bypass graft patency.
  A normal CTCA has a very high negative predictive value.
• Coronary artery calcium score: A quick non-contrast scan. A score of zero means a very low risk of events. It is used to refine cardiovascular risk and decide on preventive treatment.
• Requirements:
  • A slow, regular heart rate (beta-blockers or ivabradine beforehand).
  • Breath-holding.
  • IV contrast (check kidney function and allergy).
  Image quality is reduced in AF, heavy calcification and obesity.
• FFR-CT: Computer analysis of CTCA images that estimates whether a narrowing limits blood flow — this can reduce unnecessary invasive angiograms.
• Other cardiac CT uses: TAVI planning; left atrial anatomy before AF ablation; pericardial calcification; aortic disease.

Functional (Stress) Imaging

Functional tests show whether a narrowing actually causes ischaemia. NICE recommends them when CTCA shows disease of uncertain significance, or for people with known coronary disease.

• Stress echocardiography — exercise or dobutamine. Wall motion abnormalities under stress. No radiation.
• Myocardial perfusion scintigraphy (SPECT) — a radioactive tracer (technetium) at rest and under stress (exercise, adenosine or regadenoson). Areas of poor uptake under stress mean ischaemia; fixed defects mean scar.
• Stress perfusion cardiac MRI (adenosine) — perfusion defects plus scar imaging in one test, without radiation. Very accurate.
• Vasodilator stress (adenosine, regadenoson):
  • Avoid in severe asthma and high-grade AV block.
  • Stop caffeine and theophyllines for 12–24 hours beforehand (they block the effect).
• Dobutamine stress: Avoid with severe hypertension or significant arrhythmias.

Cardiac MRI

Why it is special: Cardiac MRI gives the most accurate measurement of chamber size and EF, and uniquely shows tissue character — scar, inflammation, fat, iron and infiltration.

• Late gadolinium enhancement (LGE) — the pattern of scar suggests the cause:
  • Subendocardial or transmural, in a coronary territory — infarction.
  • Mid-wall stripe — dilated cardiomyopathy.
  • Patchy — HCM (at RV insertion points).
  • Subepicardial or patchy — myocarditis; sarcoidosis.
  • Diffuse subendocardial, with abnormal gadolinium handling — amyloidosis.
• T2 imaging and mapping — oedema (acute myocarditis, acute MI, Takotsubo).
• T2* imaging — iron overload (thalassaemia, haemochromatosis).
• T1 mapping and extracellular volume — diffuse fibrosis, amyloid, Fabry disease (low T1).
• Other uses:
  • Viability — will a damaged area recover after revascularisation?
  • Congenital heart disease.
  • Pericardial disease.
  • Cardiac masses.
  • Aorta.
  • Stress perfusion.
• Limitations:
  • Long scan; claustrophobia.
  • Some devices are not MRI-conditional (check pacemakers and ICDs).
  • Gadolinium caution in severe CKD.
  • Arrhythmia degrades images.

Nuclear Cardiology and PET

• Bone scintigraphy (DPD or PYP scan) — for ATTR cardiac amyloidosis:
  • Strong cardiac uptake (Perugini grade 2–3), together with no monoclonal protein in the blood and urine (serum free light chains, immunofixation), diagnoses ATTR without a biopsy.
  • A monoclonal protein must be excluded, because AL amyloid can also take up the tracer.
• MUGA scan (radionuclide ventriculography) — reproducible EF measurement. Historically used for chemotherapy monitoring; now often replaced by echo or MRI.
• FDG-PET:
  • Cardiac sarcoidosis (inflammation) — needs a special diet beforehand to suppress normal heart uptake.
  • Prosthetic valve and device infection.
  • Large-vessel vasculitis.
  • Viability.
• SPECT perfusion imaging — see Functional (Stress) Imaging.

Invasive Coronary Angiography

• What it is: Catheters passed from the wrist (radial — preferred, fewer bleeding complications) or groin (femoral) into the coronary arteries. Contrast shows any narrowing, and angioplasty and stenting (PCI) can be done at the same time.
• Indications:
  • STEMI (primary PCI) and high-risk NSTEMI.
  • Angina not controlled by drugs.
  • Inconclusive non-invasive tests.
  • Before valve surgery.
  • Unexplained heart failure.
  • Survivors of cardiac arrest.
• Physiological assessment:
  • Fractional flow reserve (FFR) or iFR — a pressure wire measures whether a narrowing limits flow.
  • FFR of 0.80 or less means significant — PCI improves outcomes.
• Intracoronary imaging (IVUS, OCT) — plaque detail, sizing stents, SCAD.
• Microvascular and spasm testing (acetylcholine, adenosine) — for angina with normal coronaries (INOCA).
• Complications (about 1 in 1,000 serious):
  • Access-site bleeding, haematoma, pseudoaneurysm.
  • Contrast nephropathy (hydrate; check renal function).
  • Contrast allergy.
  • Stroke.
  • MI, coronary dissection.
  • Arrhythmias.
  • Death.
• Before the procedure:
  • Hold metformin around the procedure if kidney function is impaired.
  • Manage anticoagulants.
  • Check kidney function and allergies.