Cardiovascular Medicine

Hypertension

(aligned with NICE NG136 2023)

1 Why it matters

Systemic hypertension is the leading modifiable cause of premature death worldwide, accounting for roughly half of all cardiovascular deaths.
In the UK it affects >25 % of adults; prevalence rises with age and obesity, yet many individuals remain undiagnosed because the condition is usually silent.
Effective detection and treatment reduces risk of stroke, myocardial infarction, heart failure, chronic kidney disease (CKD) and dementia.

2 Definitions & diagnostic thresholds

Setting	Threshold to investigate further	Threshold to offer treatment
Clinic (seated, validated device)	≥140/90 mm Hg	Persistent ≥140/90 mm Hg and mean home/ABPM ≥135/85 mm Hg
Home BP or 24 h Ambulant Monitoring (ABPM)	≥135/85 mm Hg	≥135/85 mm Hg (or ≥130/80 mm Hg if <65 yrs or CV/renal risk)

White-coat hypertension = raised clinic readings with normal ABPM (<130/80 mm Hg daytime average); advise lifestyle measures and repeat monitoring.

Malignant (accelerated) hypertension = rapid BP rise usually >180/120 mm Hg with retinal haemorrhages ± papilloedema or acute end-organ injury—treat as emergency.

3 Classification by aetiology

Primary (“essential”) hypertension – ~95 %
Multifactorial: advancing age, family history, African/Caribbean ancestry, obesity, high-salt diet, alcohol excess, stress, inactivity.
Secondary hypertension – ~5 %: suspect if onset <30 yrs, abrupt/severe rise, resistant to ≥3 drugs, or electrolyte abnormalities.
Renal: CKD, glomerulonephritis, polycystic kidneys, renovascular disease (atherosclerosis in older smokers; fibromuscular dysplasia in young females).
Endocrine: primary hyperaldosteronism (Conn), phaeochromocytoma, Cushing, acromegaly, thyrotoxicosis, hyperparathyroidism.
Vascular/anatomical: coarctation of aorta.
Drugs & toxins: NSAIDs, corticosteroids, oral contraceptives, cyclosporin, erythropoietin, cocaine, amphetamines, liquorice.
Pregnancy-related: pre-eclampsia, gestational hypertension.

4 Key pathophysiology points (high-yield)

Renin-angiotensin-aldosterone-system (RAAS) overactivity drives arteriolar vasoconstriction and sodium–water retention.
Renal artery stenosis → reduced perfusion → renin surge → secondary hyperaldosteronism; affected kidney atrophies while contralateral kidney may enlarge.
Sustained pressure causes medial hypertrophy and fibroelastic intimal thickening of arteries/arterioles → progressive end-organ damage.
Malignant hypertension causes fibrinoid necrosis of arterioles with microangiopathic haemolysis; presents with encephalopathy, pulmonary oedema, rapidly rising creatinine.

5 Clinical presentation

Symptoms – usually none; occasional morning headache, visual disturbance, epistaxis in severe disease.
Signs – measure BP in both arms, check height/weight, look for:
Retinopathy (silver/copper wiring → haemorrhages/cotton-wool spots → papilloedema).
Radio-femoral delay or weak femorals (coarctation).
Renal bruits, displaced apex (LVH), thyromegaly, cushingoid features.
Evidence of target-organ damage: LV heave, ankle oedema, neuro-cognitive changes.

6 Assessment & investigations

Purpose	Investigation	Interpretation / action
Confirm diagnosis	ABPM (≥14 daytime readings) or 4 days of home BPs (≥2 readings × morning & evening)	Treat if mean ≥135/85 mm Hg (or ≥130/80 mm Hg high-risk)
Baseline & risk stratification	Fasting glucose/HbA1c, lipid profile, U\&E, creatinine/eGFR, urinalysis (blood ± ACR), cardiovascular risk calculator (QRISK3)	Guides statin/antiplatelet decisions
End-organ damage	ECG (LVH, prior MI), transthoracic echo if murmur/HF, fundoscopy, urine ACR	Worsens prognosis → aggressive control
Screen secondary causes	U\&E (hypokalaemia), plasma renin/aldosterone ratio, urinary catecholamines, calcium, TFTs; renal duplex Doppler, CT/MR angiography for stenosis; cortisol tests if Cushing	Treat underlying disease
Pre-treatment safety	U\&E before ACE-i/ARB/diuretic; repeat within 2 weeks of initiation or dose change	Stop / adjust if creatinine rises >30 % or K⁺ > 5.5 mmol/L

7 Management (NICE NG136)

Lifestyle optimisation (all patients)
- Weight reduction (target BMI 20–25 kg/m²).
- Daily moderate-intensity exercise ≥150 min/week.
- Sodium restriction <6 g salt/day; high-potassium DASH-style diet.
- Limit alcohol to ≤14 units/week, smoke cessation, caffeine moderation.
Pharmacological therapy – stepwise approach
- Step 1 – initiate if persistent hypertension + target-organ damage, established CVD, renal disease, diabetes, 10-yr CV risk ≥10 % or age <80 with sustained BP ≥160/100 mm Hg)*
  - Age <55 yrs & non-black ethnicity: ACE-i (e.g., lisinopril 10 mg OD, max 40 mg) or ARB (e.g., candesartan 8 mg OD, max 32 mg).
  - Age ≥55 yrs or African/Caribbean origin (any age): CCB (e.g., amlodipine 5 mg OD, max 10 mg). Use thiazide-like diuretic if CCB not tolerated.
- Step 2 – add the drug from the alternate class (ACE-i/ARB + CCB)
- Step 3 – add thiazide-like diuretic (indapamide MR 1.5 mg OD or chlortalidone 12.5 mg-25 mg OD)
- Step 4 (Resistant HTN) – if K⁺ ≤ 4.5 mmol/L, add spironolactone 25 mg OD (monitor U\&E at 1 & 4 weeks, then 3-monthly). If K⁺ > 4.5 mmol/L or spironolactone contraindicated, add α-blocker (doxazosin MR 4 mg OD, max 16 mg) or β-blocker (bisoprolol 5 mg OD, max 20 mg). Consider specialist referral.

*Treat people >80 yrs if clinic BP ≥150/90 mm Hg; aim <150/90 mm Hg (<145/85 home).

Adjuncts

Offer atorvastatin 20-80 mg OD if QRISK3 ≥10 % or established CVD.
Low-dose aspirin only if existing CVD or secondary prevention.

Monitoring

Home/clinic BP every 4-6 weeks after drug changes until stable, then at least annually.
U\&E: 1-2 weeks after starting ACE-i/ARB/thiazide/spironolactone; every 6-12 months thereafter.
Glycaemic & lipid profile annually.

Hypertensive emergencies

Admit for IV therapy if BP > 180/120 mm Hg plus acute organ injury (encephalopathy, pulmonary oedema, aortic dissection, eclampsia).
Reduce mean arterial pressure by no more than 25 % in first 24 h.
Typical choices: IV labetalol infusion, IV hydralazine (pregnancy), IV sodium nitroprusside in ITU.
Start long-term oral regimen once stable.

Special situations

Pregnancy (NICE NG133) – treat persistent BP ≥ 140/90 mm Hg with labetalol first-line; nifedipine MR or methyldopa alternatives. Avoid ACE-i/ARB/diuretics.
Chronic kidney disease – prefer ACE-i/ARB regardless of age or ethnicity; target clinic BP < 130/80 mm Hg if ACR ≥ 70 mg/mmol.
Diabetes mellitus – ACE-i/ARB first-line; tighter targets reduce microvascular complications.
Black ethnicity – combination of CCB + ARB often needed; avoid ACE-i monotherapy due to low renin physiology.
Older frail patients – treat if symptomatic or BP ≥ 160/90 mm Hg; individualise targets to balance falls risk.

8 Technique for accurate BP measurement (pearls)

Use validated automatic device with appropriate cuff (bladder width >40 % arm circumference).
Patient seated, feet flat, arm supported at heart level, rest >5 min.
Take at least two readings ≥1 min apart; average additional readings if difference >10 mm Hg.
Document which arm, patient position and Korotkoff phases used for systolic/diastolic if manual.

9 Complications to anticipate

Cardiac – LVH, heart failure with preserved or reduced EF, coronary artery disease, sudden death.
Neurological – ischaemic & haemorrhagic stroke, vascular dementia, intracerebral haemorrhage.
Renal – CKD, proteinuria, nephrosclerosis, ESRD.
Ophthalmic – retinal artery/vein occlusion, hypertensive retinopathy leading to vision loss.
Vascular – aortic dissection, peripheral arterial disease.

10 Key follow-up points

Annual review including BP, cardiovascular risk, medication adherence, lifestyle.
Encourage validated home BP monitors and diary.
Discuss fertility plans in women of child-bearing age; review drugs pre-conception.
Re-evaluate secondary causes if control suddenly deteriorates or new suggestive features appear.

Take-home message:

Hypertension is common, silent and lethal – but eminently treatable.
Diagnose with ABPM or home readings, address lifestyle early, and escalate pharmacotherapy methodically.
Target < 140/90 mm Hg in most; lower thresholds for high-risk groups.
Rigorous monitoring and patient empowerment underpin long-term success.

Angina (Stable Angina Pectoris)

(aligned with NICE CG126 Stable Angina: Management 2016)

1 Why it matters

Coronary ischaemia remains the single biggest cause of premature death in the UK; roughly 2 million people live with stable angina and face an annual MI/death risk of ≈ 3–4 % despite modern therapy.
Early recognition and optimal treatment halve the chances of progressing to acute coronary syndrome (ACS) and markedly improve quality of life.
Every angina consultation is an opportunity to modify global cardiovascular risk (lipids, blood pressure, smoking, glycaemic control).

2 Pathophysiology – high yield

Atherosclerotic plaque causing ≥ 70 % luminal narrowing curtails flow reserve; during exertion the oxygen demand of myocardium outstrips supply, producing sub-endocardial ischaemia.
Myocyte ATP depletion → adenosine & lactate trigger cardiac nociceptors → characteristic pain.
Variant (Prinzmetal) episodes arise from transient epicardial spasm on a background of endothelial dysfunction or stimulant use.
Unstable angina results from plaque rupture with non-occlusive thrombus; risk of transmural infarction is high without escalation of therapy.
Supply–demand mismatch (severe anaemia, thyrotoxicosis, tachyarrhythmia, severe AS/HCM) can unmask symptoms despite unobstructed coronaries.

3 Risk factors & aetiology

Non-modifiable: age > 55 years, male sex, family history of premature CAD.
Modifiable: smoking, hypertension, dyslipidaemia, diabetes, obesity, sedentary lifestyle, chronic kidney disease.
Other causes/precipitants: coronary spasm, microvascular disease (cardiac syndrome X), severe anaemia, stimulant drugs.

4 Clinical presentation

Angina:
- Constricting/heavy central discomfort ± radiation to jaw/arms;
- Precipitated by exertion or emotional stress;
- Relieved within ≤ 5 min by rest or glyceryl trinitrate (GTN).
- 3/3 above features present = typical angina
- 2/3 above features present = atypical angina
- ≤ 1/3 above features present = non-anginal chest pain
Often associated with dyspnoea, nausea, diaphoresis or presyncope – these are common
If the pain is continuous, pleuritic, positional or palpation-induced, then this argues against angina.
Unstable pattern: crescendo frequency/intensity, rest pain or nocturnal symptoms – treat as ACS.
Variant angina: episodic rest pain (often night/early morning) with transient ST-elevation or depression that resolves rapidly with nitrates.

5 Classification

Stable (effort) angina – predictable threshold, good prognosis on therapy.
Unstable (crescendo) angina – accelerating or rest pain; high-risk ACS spectrum.
Decubitus angina – triggered by lying flat (↑ venous return).
Variant / Prinzmetal – vasospastic, usually younger smokers or stimulant users.

6 Investigations & diagnosis

Baseline bloods: FBC, U&E/eGFR, HbA1c, lipid profile, TSH (rule out anaemia, renal disease, diabetes, thyroid disease).
Resting ECG often normal; look for Q-waves, ST-depression or T-wave inversion.
First-line anatomical test (NICE CG95 pathway): CT coronary angiography (CTCA). If inconclusive/unavailable → functional imaging (stress echo, perfusion SPECT, stress CMR).
Invasive coronary angiography when non-invasive tests are indeterminate or symptoms persist despite optimal therapy.
Always exclude ACS if pain occurs at rest or is prolonged (> 20 min) with repeat ECG/troponin.

7 Management

Address reversible triggers

Correct anaemia, treat thyrotoxicosis, control tachyarrhythmias, manage severe valvular disease.

Lifestyle & secondary prevention (every patient)

Lifestyle: Smoking cessation, Mediterranean-style diet, weight optimisation (BMI 20–25 kg m²), ≥ 150 min/week moderate exercise, limit alcohol ≤ 14 units/week.
Aspirin 75 mg OD lifelong (clopidogrel 75 mg OD if aspirin-intolerant).
Atorvastatin 80 mg OD (20 mg if > 75 yrs or eGFR < 30 mL/min).
Ramipril 2.5 mg → 10 mg OD (or other ACE-i/ARB) if diabetes, hypertension, LV dysfunction or CKD.

PRN symptom relief

GTN 400–800 µg sublingual; repeat after 5 min. Call 999 if pain persists > 10 min (two doses).

First-line anti-anginal (choose one)

β-blocker e.g. bisoprolol 5 mg OD (titrate 1 week to 10 mg; aim HR 55–60 bpm).
Rate-limiting CCB e.g. diltiazem MR 200 mg OD → 360 mg (avoid β-blocker + verapamil/diltiazem combo).

If monotherapy inadequate/intolerant → combine β-blocker with dihydropyridine CCB (amlodipine 5 mg OD → 10 mg) or vice-versa.

Second-line / add-on agents

Long-acting nitrate: isosorbide mononitrate 30–60 mg OD (ensure ≥ 8 h nitrate-free interval).
Nicorandil 10 mg BD → 30 mg BD (CI: acute pulmonary oedema, hypotension).
Ranolazine 375 mg BD → 750 mg BD (caution if CrCl < 30 mL/min or QTc > 500 ms).
Ivabradine 5 mg BD → 7.5 mg BD (sinus rhythm only, resting HR ≥ 70 bpm).

Variant (vasospastic) angina

Stop smoking; correct low magnesium.
CCB (amlodipine 5–10 mg OD or diltiazem MR 240 mg OD) ± long-acting nitrate.
Avoid non-selective β-blockers (as well as triptans and cocaine); prognosis excellent with therapy.

Revascularisation

Offer if symptoms persist despite optimal drugs or anatomy confers survival benefit (left main ≥ 50 %, three-vessel disease, proximal LAD).
- PCI with drug-eluting stent: dual antiplatelet therapy (aspirin 75 mg OD + clopidogrel 75 mg OD) for 12 months.
- CABG: preferred for complex multivessel or diabetic disease; slower recovery but fewer repeat procedures.

8 Monitoring & follow-up

Review symptom burden, BP/HR and drug tolerance 2–4 weeks after any dose change, then 6–12 monthly once stable.
U&E 1–2 weeks after initiating/up-titrating ACE-i, diuretic or nicorandil; repeat 6-monthly.
Lipids & HbA1c at 3 months, then annually.
Provide GTN refill reminders (bottles expire 8 weeks after opening) and a written “pain > 10 min → call 999” plan.
Encourage home BP and symptom diary; refer back if pain pattern changes to consider ACS or revascularisation.

9 Complications

Progression to ACS / MI, sudden cardiac death, heart failure, life-limiting arrhythmias.
Psychological impact: anxiety, depression; consider cardiac rehabilitation and support groups.

10 Take-home message

Stable angina signals underlying coronary disease yet offers a window for decisive prevention.
Diagnose promptly (CTCA first), tackle lifestyle and risk factors, start aspirin, statin and an anti-anginal, then escalate systematically.
Reassess regularly; refer early for PCI/CABG if symptoms or anatomy warrant.

Acute Coronary Syndromes (ACS)

(aligned with NICE NG185 Acute coronary syndromes 2020)

1 Why it matters

ACS (unstable angina, NSTEMI, STEMI) causes >100 000 UK admissions and ≈15 000 in-hospital deaths yearly; half occur within two hours of symptom onset.
Prompt reperfusion halves infarct size, preserves left-ventricular function and improves five-year survival.
Every event is a red-flag for future cardiovascular disease—aggressive secondary prevention prevents recurrent MI, stroke and heart-failure admissions.

2 Definitions & spectrum

Unstable angina: ischaemic chest discomfort ± ECG changes without biomarker rise (i.e. normal Troponin)
NSTEMI: troponin-positive ACS without ST-elevation (but other ECG changes such as ST-depression or T-wave inversion may be present).
STEMI: ST-elevation (or new LBBB / posterior leads V7-V9) plus troponin rise.
Universal MI types:
- Type 1 atherothrombotic plaque rupture (classic).
- Type 2 supply–demand mismatch (sepsis, tachyarrhythmia, anaemia, spasm).
- Types 3-5 sudden death, PCI-related, CABG-related respectively.

3 Pathophysiology – high-yield bullets

Ruptured coronary plaque → platelet plug → fibrin-rich thrombus → abrupt flow cessation.
Sub-endocardium infarcts first (NSTEMI); sustained occlusion produces transmural necrosis with ST-elevation.
Reperfusion injury: calcium influx + free radicals cause contraction-band necrosis.

4 Risk factors & epidemiology

Non-modifiable: age > 55 y, male, premature family history.
Modifiable: smoking, hypertension, T2DM, dyslipidaemia, obesity, sedentary lifestyle, cocaine use.
Women, older adults and diabetics have more silent or atypical presentations.

5 Clinical presentation

Severe central or epigastric pressure lasting > 20 min, radiating jaw/arm, ± nausea, sweating, dyspnoea or palpitations. Pain not relieved by GTN.
Silent / atypical ACS may show syncope, pulmonary oedema or acute confusion.
Examination: pallor, diaphoresis, 4th heart sound; look for heart-failure signs, new pansystolic murmur (papillary rupture) or hypotension (RV infarct).

6 Assessment & investigations

12-lead ECG within 10 min: hyper-acute T waves → ST-elevation → Q-waves (STEMI); ST-depression/T-inversion or normal (NSTEMI/UA).
High-sensitivity troponin-T/I at presentation and 3 h (repeat at 6-12 h if suspicion remains). Rise/fall > 20 % or level > 99th centile = myocardial injury.
CXR (exclude aortic dissection, pulmonary oedema) but do not delay treatment.
Bloods: FBC, U&E, eGFR, glucose/HbA1c, lipids, coagulation.
Risk stratify non-ST-elevation cases with GRACE score (≥140 = very high risk).
Echo for regional wall-motion abnormality (diagnosis & complications).
Coronary angiography timing: immediate (<2 h) if haemodynamic/arrhythmic instability; <24 h if GRACE > 140; <72 h if GRACE 109-140.

7 Immediate management pathway

A. Universal first measures

Oxygen only if SpO₂ < 94 % or cardiogenic shock.
Morphine 2.5-5 mg IV + metoclopramide 10 mg IV for pain.
GTN 400-800 µg SL (repeat after 5 min).
Aspirin 300 mg chewable plus ticagrelor 180 mg PO load (or clopidogrel 600 mg if ticagrelor contraindicated).
Anticoagulation:
- STEMI – unfractionated heparin 60 IU/kg IV (max 5 000 IU) before PCI
- NSTEMI/UA – fondaparinux 2.5 mg SC OD or enoxaparin 1 mg kg⁻¹ BD (OD if eGFR < 30 mL min⁻¹).

B. Reperfusion

STEMI: primary PCI within 120 min of first medical contact. If delay > 120 min, give fibrinolysis (tenecteplase weight-based IV bolus) and transfer for rescue PCI if ECG unchanged at 90 min.
NSTEMI/UA: medical stabilisation + invasive strategy per GRACE above.

8 Hospital care & secondary prevention

Pharmacotherapy (start within 24 h unless contraindicated)

Dual antiplatelet therapy (DAPT): continue aspirin 75 mg OD lifelong + ticagrelor 90 mg BD (or prasugrel 10 mg OD / clopidogrel 75 mg OD) for 12 months.
β-blocker: bisoprolol 2.5-10 mg OD (aim HR 55-60 bpm).
ACE-i: ramipril 2.5 mg BD → 5 mg BD, titrate to 10 mg BD; check U&E at 1 & 3 weeks.
High-dose statin: atorvastatin 80 mg OD (20 mg if > 75 y or severe CKD).
Aldosterone antagonist: eplerenone 25 mg OD (→ 50 mg) if EF < 40 % and either diabetes or heart failure—start ≥ 24 h post-MI.
PPI cover (e.g. lansoprazole 30 mg OD) in patients on DAPT ± oral anticoagulant.

Monitoring

Daily ECG, pulse, BP for 48 h; telemetry if high-risk arrhythmia.
Serial U&E, creatinine, K⁺ at baseline, day 1, and after each drug titration.
Echo before discharge to assess EF; repeat at 6-12 weeks if LV dysfunction.

9 Complications to anticipate

Arrhythmias: VF/VT mostly within 24 h, treat with DC shock ± amiodarone; high-grade AV block after inferior MI may require pacing.
Cardiogenic shock (large anterior MI).
Mechanical rupture (papillary muscle day 3-5 → acute MR; septal or free-wall rupture day 5-7 → tamponade).
Pericarditis (early fibrinous, or Dressler syndrome 1-3 weeks – give NSAID).
LV aneurysm / mural thrombus (after week 4) – consider warfarin 3 months.

10 Discharge & long-term follow-up

Cardiac rehabilitation within 10 days: exercise, diet, smoking cessation, psychological support.
Driving: Group 1 licence – resume 1 week after successful PCI, or 4 weeks after uncomplicated ACS managed medically; Group 2 must inform DVLA and undergo functional testing after 6 weeks.
Work: graded return guided by occupational demand, typically 2-4 weeks for sedentary roles.
Clinic review at 2 weeks, 6 weeks, then every 6-12 months: symptom status, BP, lipids (non-HDL-C target < 2.6 mmol L⁻¹), HbA1c if diabetic, drug adherence.
Stress testing or CT-coronary angiography if post-MI angina persists.

11 Take-home message

Acute coronary syndromes demand fast diagnosis, rapid reperfusion and lifelong prevention.
Give aspirin immediately, activate the cath lab without delay for STEMI, and risk-stratify NSTEMI with GRACE.
Start high-dose statin, ACE-i, β-blocker, DAPT and cardiac rehab before discharge.
Vigilant monitoring for arrhythmias and mechanical complications saves lives; equally, robust secondary prevention and lifestyle change keep those lives healthy.

Narrow-Complex Tachycardia (Supraventricular Tachycardia)

(aligned with 2019 ESC “Supraventricular Tachycardia” guideline and UK Resuscitation Council Advanced Life Support Tachycardia Algorithm)

1 Why it matters

Narrow-complex tachycardias (NCT) account for ≈0.2 % of the UK population and are the commonest symptomatic arrhythmias in young adults. Most are benign, but rapid rates may cause syncope, myocardial ischaemia or tachycardia-induced cardiomyopathy.
In patients with an accessory pathway, pre-excited atrial fibrillation can degenerate into ventricular fibrillation in minutes. Early recognition and decisive treatment are therefore lifesaving.

2 Definition & classification

NCT = HR > 100 bpm + QRS < 120 ms; activation therefore travels through the normal His–Purkinje system.
Regular rhythms:
- sinus tachycardia
- atrioventricular nodal re-entry tachycardia (AVNRT)
- atrioventricular re-entry tachycardia via an accessory pathway (AVRT)
- typical atrial flutter with fixed block
- focal atrial tachycardia
- junctional tachycardia.
Irregular rhythms:
- atrial fibrillation
- atrial flutter with variable block
- multifocal atrial tachycardia
- sinus arrhythmia.

3 Pathophysiology – high yield

Re-entry circuits:
- AVNRT (≈80 %) uses dual AV-nodal pathways
- AVRT traverses an accessory pathway (orthodromic → narrow QRS).
Macro-re-entry round the right-atrial cavotricuspid isthmus generates the classic 300-bpm typical flutter saw-tooth pattern.
Focal automaticity or micro-re-entry causes atrial tachycardia; increased sympathetic drive explains physiological sinus tachycardia.
Holiday-heart syndrome: binge alcohol (or cannabis) precipitates SVT or new-onset AF in structurally normal hearts.

4 Aetiology & precipitants

Structural: ischaemic heart disease, cardiomyopathy, post-surgery scar, congenital accessory pathways (WPW).
Functional/triggered: fever, pain, pregnancy, anaemia, pulmonary embolism, hyper-thyroidism, β-agonists, caffeine, nicotine, alcohol excess.
Electrolyte / endocrine: hypokalaemia, hypomagnesaemia, thyrotoxicosis; treatable precipitants must always be sought.

5 Clinical features

Sudden-onset, fast, regular palpitations ± chest tightness, dyspnoea, light-headedness.
Haemodynamic compromise: hypotension, syncope, pulmonary oedema – mandate immediate synchronised cardioversion.
Sustained high rates over weeks can lead to reversible LV dysfunction (tachycardia-induced cardiomyopathy).

6 Assessment & investigations

12-lead ECG during the episode (or rhythm strip) – classify regular vs irregular; look for P-wave/RP relationship or flutter waves.
Baseline tests: FBC, U&E, Mg²⁺, Ca²⁺, TSH, glucose, troponin if chest pain.
Echocardiography to rule out structural disease; ambulatory monitor or implantable loop recorder when episodes are infrequent.
Consider electrophysiology study (EPS) in recurrent, poorly defined, or ablation-planned cases.

7 Acute management algorithm

Always treat apparent cause first (pain, hypovolaemia, sepsis, electrolyte disturbance).

A. Haemodynamic instability (syncope, shock, chest pain, acute HF) → Synchronised DC cardioversion up to 3 escalating shocks.

B. Stable, regular NCT (probable AVNRT/AVRT)

Vagal manoeuvre: modified Valsalva or carotid sinus massage (contra-indication: carotid bruit). Success ≈25 %.
Adenosine IV: 6 mg rapid bolus → flush; if no conversion in 1–2 min give 12 mg; may repeat 12 mg once (max 30 mg). Warn of transient flushing/“impending doom”. Avoid in asthma—use verapamil 2.5–5 mg IV over 2 min instead (repeat up to 15 mg).
β-blocker (esmolol 500 µg kg⁻¹ over 1 min → infusion 50–200 µg kg⁻¹ min⁻¹) if adenosine/CCB contra-indicated.
If rhythm unmasks typical flutter → proceed to rate control (diltiazem/verapamil) or elective DC cardioversion.

C. Irregular NCT

New-onset AF/flutter <48 h: rate vs rhythm control per AF guideline; consider anticoagulation.
Pre-excited AF (delta wave during sinus; RR wildly variable): do not give AV-nodal blockers – use flecainide 2 mg kg⁻¹ IV over 10 min or urgent cardioversion.

8 In-hospital care & monitoring

Continuous cardiac monitoring for ≥ 6 h post-conversion.
Correct electrolytes, review QTc, stop precipitating drugs (e.g. salbutamol overuse, digoxin toxicity).
Anticoagulate atrial flutter/fibrillation if CHA₂DS₂-VASc ≥ 1 (male) or ≥ 2 (female).

9 Long-term management & secondary prevention

Lifestyle / trigger control

Limit caffeine, alcohol (holiday-heart warning), and recreational stimulants; maintain normal K⁺/Mg²⁺.

Pharmacological suppression (when ablation unsuitable or while awaiting it)

AVNRT / AVRT: daily bisoprolol 2.5–10 mg OD or diltiazem MR 240–360 mg OD; WPW patients without structural heart disease may use flecainide 50–150 mg BD.
Focal atrial tachycardia / inappropriate sinus tachycardia: trial β-blocker or ivabradine 5–7.5 mg BD.
Review drug efficacy and ECG at 6–8 weeks; adjust doses to maintain resting HR 60–80 bpm.

Catheter ablation (curative option)

First-line for AVNRT, orthodromic AVRT and typical flutter; success > 95 %, major complication < 1 %.
Consider for focal atrial tachycardia, symptomatic inappropriate sinus tachycardia, or drug-refractory AF triggers.

10 Special situations

Pregnancy: vagal manoeuvres first; adenosine safe in all trimesters; β-blocker (metoprolol) or verapamil if persistent; defer ablation until postpartum unless life-threatening.
Athletes: screen for WPW/long-QT during pre-participation ECG; asymptomatic WPW warrants electrophysiology ± prophylactic ablation in high-risk sports.

11 Complications

Syncope and trauma, tachycardia-mediated cardiomyopathy, thrombo-embolism (flutter/fibrillation), sudden death in pre-excited AF.

12 Take-home message

Narrow-complex tachycardias are rapid but usually repairable rhythms.

Think: unstable → shock; stable → vagal → adenosine → specialist drugs. Identify the circuit, abolish triggers, and offer curative catheter ablation early—patients can often be cured for life with a 30-minute lab procedure. Vigilant investigation, clear safety-netting and guideline-aligned follow-up keep recurrence, stroke and sudden death to a minimum.

Broad-Complex Tachycardia

(aligned with 2019 ESC “Supraventricular Tachycardia” guideline and UK Resuscitation Council Advanced Life Support Tachycardia Algorithm)

1 Why it matters

A sustained broad-complex tachycardia (BCT) is a medical emergency: ≈ 85 % are ventricular tachycardia (VT) and up to 30 % of VTs degenerate into ventricular fibrillation (VF) or pulseless electrical activity within minutes.
Misdiagnosing VT as a supraventricular tachycardia with aberrancy (SVTa) and giving an AV-nodal blocker may precipitate circulatory collapse.
Timely defibrillation or synchronised cardioversion restores cardiac output, limits myocardial injury and prevents sudden cardiac death.

2 Definition & core concepts

Broad complex: QRS duration > 120 ms at a ventricular rate > 100 bpm.
Main rhythms:
- Monomorphic VT – single re-entry circuit (post-MI scar, cardiomyopathy).
- Polymorphic VT / torsades de pointes – beat-to-beat axis change, always with a prolonged QTc or acute ischaemia.
- SVTa with aberrancy – any narrow-complex tachycardia conducting down a bundle-branch block.
- Antidromic AVRT (WPW) – entire ventricle activated via an accessory pathway → broad QRS.
- Pulseless VT / VF – immediately life-threatening and managed as cardiac arrest.

3 Aetiology & precipitants

Structural heart disease: previous MI scar, dilated or hypertrophic cardiomyopathy, arrhythmogenic right-ventricular cardiomyopathy, myocarditis, congenital heart disease repair scars.
Channelopathies: long-QT syndrome, Brugada, catecholaminergic polymorphic VT.
Metabolic / toxic: hypokalaemia, hypomagnesaemia, hyperkalaemia, hypoxia, acidosis, digoxin toxicity, class I/III anti-arrhythmics, macrolides, methadone, antipsychotics, cocaine.
Functional triggers: acute ischaemia, heart-failure decompensation, fever, thyrotoxicosis, sepsis.

4 Pathophysiology – high-yield bullets

Re-entry around scar creates a stable circuit → monomorphic VT.
Early after-depolarisations during prolonged repolarisation generate torsades.
Triggered activity in the Purkinje network explains outflow-tract or fascicular idiopathic VT.
AV dissociation in VT: atria and ventricles beat independently because the ventricle is no longer activated via the His–Purkinje system.

5 Clinical presentation

Sudden palpitations ± chest tightness, pre-syncope/syncope, dyspnoea or “thumping” sensation.
Haemodynamic compromise: hypotension, shock, acute pulmonary oedema, ischaemic chest pain and altered consciousness mandate immediate synchronised shock.
Pulseless VT presents as cardiac arrest (no palpable pulse despite electrical activity).

6 Diagnosis & investigations

ECG pointers favouring VT (treat as VT if uncertain)

QRS > 160 ms, extreme axis (“north-west”).
Uniform positive or negative QRS in all chest leads (concordance).
Capture or fusion beats, AV dissociation, or 2 : 1 / 3 : 1 Mobitz II pattern.
Positive QRS in aVR or bizarre morphology not matching any bundle-branch block.

Core tests

12-lead ECG during the episode (print and label).
Bloods: FBC, U&E, Mg²⁺, Ca²⁺, glucose, high-sensitivity troponin if ischaemia suspected, digoxin level if relevant.
Transthoracic echo then cardiac MRI or coronary angiography to identify scar or ischaemia.
Continuous telemetry or ambulatory Holter; implantable loop recorder for infrequent spells.
Electrophysiology study to define mechanism and guide ablation if recurrent.

7 Immediate management pathway

Assess stability (ABCDE)
- Unstable (pulse but shock, syncope, chest pain, heart-failure signs): Synchronised biphasic DC cardioversion – 150 J → 200–360 J as required.
- Pulseless: follow the VF/pVT cardiac-arrest algorithm – CPR + immediate unsynchronised shock (200 J) ×3, adrenaline 1 mg IV after 2nd shock, amiodarone 300 mg IV after 3rd shock.
Identify & correct reversible causes (Hs & Ts: hypoxia, hypo-/hyperkalaemia, hypothermia, toxins, tamponade, tension pneumothorax, thrombosis).
Stable monomorphic VT
- Amiodarone 300 mg IV over 20–60 min, then infusion 900 mg over 24 h.
- If amiodarone unavailable / contraindicated: lidocaine 1 mg kg⁻¹ IV bolus (max 100 mg) → infusion 1–4 mg min⁻¹, or procainamide 10 mg kg⁻¹ IV over 20 min (avoid if LVEF < 40 %).
Polymorphic VT / torsades de pointes
- Magnesium sulfate 2 g IV over 10 min (may repeat once).
- Overdrive pacing (temporary transvenous or isoprenaline infusion) aiming 90–120 bpm if persistent.
- Stop QT-prolonging drugs, correct K⁺ > 4.5 mmol L⁻¹, treat ischaemia.
Suspected SVTa with aberrancy
- If doubt, treat as VT.
- Avoid AV-nodal blockers (adenosine, verapamil, diltiazem) until definite narrow-complex rhythm documented.
Pre-excited AF (broad, irregular)
- Do not give AV-node blockers. Use flecainide 2 mg kg⁻¹ IV (max 150 mg) over 10 min or immediate DC cardioversion.

8 In-hospital care & monitoring

Cardiac monitoring ≥ 24 h after any VT episode or drug infusion.
Daily U&E, Mg²⁺, Ca²⁺; maintain K⁺ 4.0–5.0 mmol L⁻¹, Mg²⁺ > 0.8 mmol L⁻¹.
Serial troponin if chest-pain or post-shock; repeat echo if haemodynamics change.
Consider coronary angiography within 24 h if acute coronary syndrome suspected.
If secondary to heart-failure decompensation, optimise diuretics, ACE-i/ARNI, β-blocker and mineralocorticoid antagonist before discharge.

9 Long-term management & secondary prevention

Lifestyle / risk-factor control

Smoking cessation, weight optimisation, alcohol moderation, electrolyte vigilance, review QT-prolonging prescriptions.

Pharmacological suppression

β-blocker (bisoprolol 2.5–10 mg OD) for all with structural heart disease or channelopathy.
Amiodarone loading 200 mg TDS × 1 week → 200 mg BD × 1 week → 200 mg OD; check TFT/LFT before start, then every 6 months.
Sotalol 80 mg BD (max 160 mg BD) only if structurally normal heart and QTc < 460 ms.
Mexiletine 200 mg TDS useful for refractory scar-related VT under specialist care.

Catheter ablation

First-line curative therapy for idiopathic outflow-tract or fascicular VT.
Indicated after ≥ 2 monomorphic VT episodes despite drugs, or to reduce ICD shocks in scar-related VT. Success 70–85 %.

Implantable cardioverter-defibrillator (ICD)

Secondary prevention: survivors of VF or haemodynamically unstable VT.
Primary prevention (despite ≥ 3 months of optimal medical therapy):
- LVEF ≤ 35 % with NYHA II–III heart failure.
- LVEF ≤ 30 % > 40 days post-MI.
- Specific inherited conditions (Brugada with syncope or sustained VT, long-QT with syncope despite β-blocker, hypertrophic cardiomyopathy with risk factors).
CRT-D if QRS ≥ 130 ms with LBBB morphology + LVEF ≤ 35 % + NYHA II–IV.
Subcutaneous ICD for patients at high infection risk or without pacing requirement.

Follow-up schedule

ICD/CRT checks at 1 month, 3 months, then every 6 months (remote where available).
Drug review, electrolytes, renal profile and ECG every 6–12 months.
Cardiac rehab and psychological support to address anxiety related to shocks.

10 Complications to anticipate

Degeneration to VF, cardiogenic shock, sudden cardiac death.
Tachycardia-induced cardiomyopathy with chronic high-burden VT/V-extrasystoles.
Drug adverse effects: amiodarone-induced thyroid or liver dysfunction, sotalol torsades.
Device-related: lead fracture, infection, inappropriate shocks, pacing-induced cardiomyopathy.

11 Key follow-up pearls

Educate patients to seek urgent review for palpitations lasting > 30 min or syncope.
Provide an emergency card detailing ICD magnet response and drug allergies.
Athletes with previous VT require sports-cardiology clearance before return to competitive activity.
First-degree relatives of patients with inherited arrhythmia syndromes need ECG ± genetic counselling.

12 Take-home message

Treat every broad-complex tachycardia as ventricular until proved otherwise. If unstable, shock first; if pulseless, start CPR and defibrillate. Correct electrolytes, start β-blocker ± amiodarone, and plan early ICD or ablation according to ESC 2022 criteria. Mastering this algorithm is lifesaving on the ward, in the catheter lab and in the exam hall alike.

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