Handbook of Internal Medicine, 9th Edition (Hospital Authority, Hong Kong)

Authors, Journal, Affiliations, Type, DOI

Prepared by the Co-ordinating Committee in Internal Medicine, Hospital Authority, Hong Kong. 9th edition, 2024; version 9.1 dated June 2026.

No DOI. Available through the HA intranet and the eKG Internal Medicine portal.

Type: book (institutional clinical handbook). It is a derivative document: each section carries its own reference list pointing to primary ESC, AHA/ACC and other guidelines, generally dated 2014–2023.

Coverage. The handbook is organised by specialty. This page documents the Cardiology chapter (pp. C1–C41) and four cardiology-relevant items from other chapters: DOAC prescribing (Haematology, H14–15), and hypertension in old age, orthostatic hypotension and syncope (Geriatrics, Gr21–22, Gr30–31, Gr45–46). The remaining chapters — dermatology, endocrinology, gastroenterology, haematology beyond DOACs, immunology, infections, nephrology, neurology, palliative medicine, rehabilitation, respiratory, rheumatology, toxicology and critical care — are outside this page's scope.

Overview

A practical bedside handbook for internal medicine in the Hong Kong public hospital system, written for frontline clinicians rather than as an evidence document. Its characteristic content is operational: drug doses, infusion rates, electrical cardioversion energies, antibiotic regimens and procedure steps, laid out as algorithms and checklists rather than as graded recommendations. Most sections carry no class-of-recommendation or level-of-evidence notation at all.

For the wiki its value is complementary rather than competitive. The ESC and AHA guideline pages record what the evidence supports; this handbook records what a Hong Kong hospital does about it, including agents and doses that appear in local formularies and thresholds used to trigger consultation.

The 2026 ESC heart failure guideline ingested separately has since moved several of the positions this handbook states, most visibly the LVEF classification. Those divergences are recorded on the affected pages rather than corrected here — the handbook is a dated document and is cited as such.

Keywords

cardiopulmonary resuscitation; ACLS; defibrillation; atrial fibrillation; rate control; cardioversion; unstable angina; NSTEMI; STEMI; fibrinolysis; primary PCI; acute pulmonary oedema; hypertensive emergency; hypertensive urgency; aortic dissection; chronic heart failure; HFrEF; HFmrEF; HFpEF; pulmonary embolism; cardiac tamponade; pericardiocentesis; infective endocarditis prophylaxis; perioperative cardiovascular evaluation; DOAC; hypertension in old age; orthostatic hypotension; syncope

Key Takeaways

Cardiopulmonary resuscitation

• BLS: compression rate 100–120/min, depth 5–6 cm, 30:2 ratio. Check breathing and pulse for no more than 10 s; if a pulse is present without normal breathing, give 1 breath every 6 s. Shockable rhythms get one shock — biphasic at the manufacturer's recommendation or maximum available (e.g. 200 J), monophasic 360 J — then immediate resumption of CPR.
• ACLS: confirm tube placement by 5-point auscultation plus a confirmation device, with continuous waveform capnography. Once an advanced airway is in place, 1 breath every 6 s with continuous compressions.
• Arrest drugs: adrenaline 1 mg (10 mL of 1:10,000) every 3–5 min; amiodarone 300 mg bolus for pulseless VT/VF then 150 mg; lignocaine 1 mg/kg then 0.5–0.75 mg/kg (max 3 mg/kg); MgSO₄ 1–2 g for torsades. Intravenous or intraosseous preferred over the endotracheal route, which requires double dosing and the L-E-A-N mnemonic (lignocaine, epinephrine, atropine, naloxone).
• Post-ROSC: titrate oxygen to 92–98%, avoid hyperventilation, treat hypotension with volume or vasopressor, initiate targeted temperature management in coma, treat seizures.
• The 5H/5T reversible-cause framework is listed in full, including tamponade, tension pneumothorax, coronary and pulmonary thrombosis.
• Cited to the 2020 AHA CPR/ECC guidelines.

Arrhythmias

• Tachycardia with a pulse is split by stability, then by QRS width. Unstable: synchronised cardioversion — narrow regular 50–100 J, narrow irregular 120–200 J, wide regular 100 J, wide irregular as unsynchronised defibrillation. Sedate where time allows, and resynchronise after each shock if repeating.
• AF/flutter rate control with doses: diltiazem 0.25 mg/kg then 5–15 mg/h; verapamil 0.075–0.15 mg/kg (check BP before a second dose); metoprolol 2–5 mg up to three doses; amiodarone 300 mg over 1 h then 10–50 mg/h; digoxin to a maximum of 1.5 mg in 24 h. In impaired function (EF <40%, CHF) use digoxin or amiodarone.
• Pre-excited AF: procainamide; all AV-nodal blocking agents are to be avoided.
• Cardioversion of persistent AF requires 3 weeks of prior anticoagulation and 4 weeks after (delayed strategy). Pharmacological conversion options are listed with doses, as are the electrical energies (AF 120–200 J, flutter 50–100 J).
• Stable regular narrow-complex tachycardia: vagal manoeuvres → ATP 10 mg then 20 mg. Carotid sinus pressure is contraindicated with carotid bruits; ATP is contraindicated in asthma.
• Bradycardia: atropine 1 mg every 3–5 min to a maximum of 3 mg, then transcutaneous pacing, dopamine 5–20 µg/kg/min or adrenaline 2–10 µg/min. Atropine is explicitly not to be relied on in type II second-degree or third-degree block, where the block is likely infranodal and the patient needs pacing.

Unstable angina / NSTEMI

• Admit high-risk cases to CCU, continuous ECG monitoring, serial hs-troponin using the ESC 0h/1h algorithm, and consult cardiology for urgent angiography in refractory ischaemia or shock.
• Antithrombotic: aspirin 160–320 mg loading then 80–100 mg daily; clopidogrel 300–600 mg or ticagrelor 180 mg loading; enoxaparin 1 mg/kg q12h, or weight-banded nadroparin.
• Anti-ischaemic: nitrates (contraindicated within 24 h of sildenafil), β-blocker titrated to heart rate <70.
• Statin regardless of baseline LDL-C; ACE-I within 24 h if LVEF <40%.
• High-risk features listed include GRACE >140, dynamic ST/T change, refractory pain, shock, and established NSTEMI.

Acute STEMI

• Infarct-localisation table by lead (inferior II/III/aVF; lateral I/aVL/V6; anteroseptal V1–V3; anterolateral V4–V6; anterior V1–V6; RV V3R/V4R).
• ST-elevation thresholds are stated by age and sex: ≥2.5 mm in men <40, ≥2 mm in men ≥40, ≥1.5 mm in women in V2–V3, and ≥1 mm in other leads.
• Reperfusion decision is by time from onset: ≤12 h and PCI-eligible → primary PCI; ≤12 h not PCI-eligible but fibrinolytic-eligible → fibrinolysis; >12 h with persistent symptoms → consider angiography.
• Fibrinolytic dosing: tenecteplase weight-banded 30–50 mg, halved for age ≥75; alteplase 15 mg bolus then 0.75 mg/kg over 30 min then 0.5 mg/kg over 1 h. Contraindications are listed in full, absolute and relative, and include suspected aortic dissection.
• Signs of reperfusion: pain resolution, early CPK peak, accelerated idioventricular or nodal rhythm, and ≥50% resolution of ST elevation in the worst lead at 60–90 min. Failure triggers rescue PCI.
• Complication management covers arrhythmia (including pacing indications in AV block and the rule that wide-complex tachycardia is treated as VT until proven otherwise), pump failure with inotrope dosing, mechanical complications, and pericarditis (colchicine for post-cardiac injury syndrome, not peri-infarct pericarditis).
• Secondary prevention includes ARNI after 36 h off ACE-I, an aldosterone blocker at LVEF ≤40% with diabetes or HF, and an SGLT2 inhibitor for heart failure.

Acute pulmonary oedema

• Bed rest upright, oxygen, low-salt diet and fluid restriction; identify and treat the precipitant (arrhythmia, ischaemia, uncontrolled hypertension, chest infection).
• If BP is stable: frusemide 40–120 mg IV, IV nitrate (GTN 1 µg/kg/min), morphine 2–5 mg slow IV. If BP is not stabilised: add inotropes — dopamine 2.5–10 or dobutamine 2.5–15 µg/kg/min.
• Monitor BP, pulse, input/output, SaO₂, CVP and respiratory rate every 30–60 min.
• Escalate to non-invasive ventilation (CPAP/BiPAP) or intubation for desaturation, exhaustion or cardiogenic shock; consider mechanical circulatory support, PCI for an ischaemic cause, or valve intervention.

Hypertensive crisis

• Emergency = >180/120 mmHg with new or worsening target-organ damage. Urgency = severe elevation without acute organ damage, usually from withdrawn or non-adherent therapy, treated by restarting or intensifying oral drugs.
• Rate of reduction is the whole point. With a compelling feature (aortic dissection, eclampsia, phaeochromocytoma crisis) reduce SBP to <140 mmHg within the first hour, and to <120 mmHg in dissection. Without one, reduce SBP by no more than 25% in the first hour, to 160/100 by 2–6 h, then to normal over 24–48 h.
• IV agents with doses: labetalol 20 mg boluses to 300 mg then 0.5–2 mg/min (to 10 mg/min); nitroprusside 0.25–0.5 µg/kg/min (limit <3 µg/kg/min if eGFR <30; avoid in pregnancy and beyond 48 h); hydralazine 10–20 mg slow IV; phentolamine 5–10 mg for catecholamine crisis.
• Condition-specific cautions: avoid labetalol and β-blockers in LV dysfunction; β-blockers are contraindicated in sympathomimetic or clonidine-withdrawal crisis because of unopposed α-vasoconstriction; nitroprusside and ACE-I are avoided in pregnancy.

Aortic dissection

• Suspect with chest, back or abdominal pain plus unequal pulses (which may be absent) or acute aortic regurgitation. Diagnosis by urgent dynamic CT or MR angiography; transthoracic echo is not sensitive, transoesophageal echo is better.
• Medical therapy starts before confirmatory imaging returns: target SBP 100–120 mmHg and heart rate 60–70/min. Labetalol first; nitroprusside is not to be used while the heart rate is uncontrolled, because reflex tachycardia increases the rate of rise of aortic pressure. Diltiazem or verapamil substitute when β-blockers are contraindicated (e.g. COAD). Hydralazine and diazoxide are actively avoided for the same reflex reason.
• Arterial line on the arm with the higher pressure. Look for tamponade, severe AR, and myocardial, cerebral or renal ischaemia.
• Type A and complicated Type B go to cardiothoracic surgery; endovascular stent grafting is described as evolving for complicated Type B at high surgical risk. Intramural haematoma and penetrating aortic ulcer are managed as dissection.

Chronic heart failure

• Classification uses four categories: HFrEF LVEF ≤40%, HFmrEF 41–49%, HFpEF ≥50% with raised filling pressures, HFimpEF previous ≤40% with follow-up >40%. This is the AHA/ACC 2022 scheme, and it is the section most affected by subsequent guideline change — see Contradictions.
• Investigation: CBC, LFT, RFT, clotting, TFT, troponin/CK, iron profile; natriuretic peptides with a single rule-out of BNP <35 or NT-proBNP <125 pg/mL; ECG, CXR, echocardiography. Aetiology work-up includes CMR, CTCA, stress imaging, cardiopulmonary exercise testing, right heart catheterisation, endomyocardial biopsy, invasive angiography and genetic testing.
• HFrEF: the four foundational drugs (ACE-I or ARB, ARNI with a 36 h ACE-I washout, β-blocker — bisoprolol, carvedilol or metoprolol succinate — MRA, SGLT2i) titrated to target, plus diuretics for volume overload. Additional therapy once optimised: ivabradine (NYHA II–III, sinus rhythm, HR ≥70 on maximal β-blocker), vericiguat (LVEF <45%, recent hospitalisation or IV diuretics, raised NP), digoxin, ferric carboxymaltose for iron deficiency, AF ablation in selected patients.
• Devices: ICD at NYHA I–III, LVEF ≤35%, >1 year survival; CRT-D at LVEF ≤35% with QRS ≥150 ms, or LBBB at 130–149 ms.
• HFmrEF and HFpEF: diuretics, SGLT2i, and "other medications to be considered" — ACE-I or ARB, ARNI, MRA — plus treatment of the underlying aetiology.

Pulmonary embolism

• Investigation includes D-dimer, ABG, CXR, ECG (sinus tachycardia, S1Q3T3, RBBB, right axis deviation, P pulmonale), TTE/TEE, lower-limb Doppler, CTPA (sensitivity 91%, specificity 78%) and V/Q scan (41%/97%), with Wells or revised Geneva pretest probability.
• Risk stratification is haemodynamic first, then RV dysfunction on imaging, troponin, and PESI.
• Anticoagulation: LMWH preferred (enoxaparin 1 mg/kg q12h if CrCl >30); unfractionated heparin for severe renal failure, likely need for rapid reversal, or unreliable subcutaneous absorption. DOAC regimens are given per agent, including the parenteral lead-in requirements for dabigatran and edoxaban.
• Haemodynamically significant PE: ICU, cautious fluids, vasopressors, ECMO; systemic thrombolysis with rtPA 100 mg over 2 h; surgical embolectomy or catheter-directed therapy if deteriorating or thrombolysis contraindicated. IVC filter for recurrence on adequate anticoagulation or absolute contraindication to it.

Cardiac tamponade

• Defined by a pericardial effusion compressing chambers to the point of haemodynamic compromise; an acute effusion of only ~200 mL can tamponade because the pericardium cannot distend.
• Causes: neoplastic, pericarditis, uraemia, iatrogenic instrumentation, trauma, acute pericarditis on anticoagulants, idiopathic.
• Signs: pulsus paradoxus, raised JVP with prominent x descent, Kussmaul's sign, hypotension, clear chest. ECG shows low voltage, tachycardia and electrical alternans; CXR shows an enlarged silhouette above ~250 mL with clear lung fields; echo shows RA/RV/LA collapse, a distended IVC and exaggerated respiratory variation in tricuspid and mitral inflow.
• Management: volume expansion; avoid positive-pressure ventilation where possible, because it further impairs filling; echo-guided pericardiocentesis; open drainage with pericardial biopsy for recurrence. The handbook's bolded warning is that misdiagnosing tamponade as congestive heart failure and giving diuretics, ACE-I or vasodilators can be lethal.

Antibiotic prophylaxis for infective endocarditis

• Restricted to the highest-risk groups before dental procedures involving gingival or periapical manipulation or oral mucosal perforation: prosthetic valve or prosthetic material (including transcatheter valves and annuloplasty rings or clips), durable mechanical circulatory support, previous or recurrent IE, defined congenital heart disease subsets (unrepaired cyanotic CHD, repaired CHD with prosthetic material for 6 months, residual shunt or regurgitation, surgical or transcatheter pulmonary valve), and cardiac transplant recipients with valvulopathy.
• Regimens: amoxicillin 2 g orally; ampicillin 2 g IM/IV or cefazolin/ceftriaxone 1 g IM/IV if oral route impossible; cephalexin 2 g, azithromycin/clarithromycin 500 mg or doxycycline 100 mg if penicillin-allergic; cefazolin or ceftriaxone 1 g if penicillin-allergic and non-oral. Vancomycin 15–20 mg/kg IV (max 2 g) where cephalosporins are precluded by anaphylaxis, angioedema or urticaria to penicillin.
• Clindamycin is no longer recommended as an alternative, because of more frequent and severe reactions.
• Prophylaxis is not recommended for respiratory, gastrointestinal, urogenital or skin and soft-tissue procedures unless the procedure is performed in the context of established infection — in which case the regimen should cover staphylococci (respiratory, skin) or enterococci (GI/GU).

Perioperative cardiovascular evaluation

• Three-tier predictor framework: active cardiac conditions that may defer surgery (unstable coronary syndrome, decompensated HF, significant arrhythmia, severe valvular disease), clinical risk factors (ischaemic heart disease, HF, diabetes, renal impairment), and minor predictors (age, abnormal ECG, non-sinus rhythm, low functional capacity, prior stroke, uncontrolled hypertension). Surgical risk is separately low (<1%), intermediate (1–5%) and high (>5%).
• A seven-step algorithm runs from emergency surgery through ACS, combined risk estimation, biomarkers (hsTnI, BNP/NT-proBNP), functional testing where it would change management, to revascularisation or proceeding.
• DAPT: continue aspirin if bleeding risk allows; stop ticagrelor 3–5 days, clopidogrel 5 days, prasugrel ≥7 days pre-operatively; never stop DAPT within the first month; defer elective surgery to 3–6 months (preferably 12) after PCI with recent MI or high ischaemic risk, and at least 1 month (preferably 6) otherwise.
• DOAC interruption is tabulated by agent, creatinine clearance and bleeding risk, with no bridging. Full dose resumes ≥24 h after a low-bleeding-risk intervention and 48–72 h after a high-risk one. High-risk interventions are itemised.
• Disease-specific guidance covers hypertension, cardiomyopathy and HF (HOCM avoids volume reduction and catecholamines), the four valve lesions with LVEF and dimension thresholds, prosthetic valves, arrhythmia, pacemakers and ICDs. Pertinent device points: reprogramme to AOO/VOO/DOO when the diathermy site is above the umbilicus and the patient is pacing-dependent; leadless pacemakers do not respond to a magnet; deactivated ICDs require continuous monitoring and external defibrillation available; place defibrillation paddles >12 cm from the generator.
• β-blockers: continue in patients already taking them; consider starting before high-risk surgery in patients with ≥2 clinical risk factors or known CAD/ischaemia.

Direct oral anticoagulants

• Dosing table by indication (post-orthopaedic VTE prophylaxis, non-valvular AF, DVT/PE treatment) for dabigatran, rivaroxaban, apixaban and edoxaban, including the renal bands and the apixaban dose-reduction criteria (2.5 mg BD with any two of age ≥80, weight ≤60 kg, creatinine ≥132.6 µmol/L).
• Interruption before procedures tabulated by agent and CrCl with low/high bleeding risk columns. Neuraxial anaesthesia may require longer cessation — consult the anaesthetist.
• Reversal: idarucizumab 2.5 g × 2 for dabigatran; andexanet alfa not available in Hong Kong at the time of writing, with four-factor prothrombin complex concentrate 2,000 units or 50 units/kg as the alternative for the factor Xa inhibitors. Dabigatran is dialysable; the others are not, being highly protein-bound. Oral activated charcoal if ingestion was <2 h.

Hypertension in old age

• Isolated systolic hypertension predominates; vascular stiffening makes older patients vulnerable to hypotension on postural change, after meals and during volume contraction, and antihypertensives increase fall risk.
• Targets: <150 mmHg systolic is strongly evidenced; 130–140 mmHg may be considered for the biologically young 65–80 with little comorbidity, while >80 or multimorbid patients should stay at <150. Diastolic target <90, and not below 65 in coronary disease — risk rises between 61 and 70 and further at ≤60, attributed to diastolic-dependent myocardial perfusion.
• Start low (about half the younger-adult dose) and go slow, because the first one to two months of therapy carries increased falls and hip fracture risk. Clinical judgement over guideline in frail patients with limited life expectancy.

Orthostatic hypotension

• Definition: systolic drop ≥20 mmHg or diastolic ≥10 mmHg within 3 minutes of standing, measured after 5 minutes supine then at 1 and 3 minutes standing; head-up tilt if the active stand is negative.
• A heart-rate-to-systolic-drop ratio <0.5 beats/min/mmHg on standing or tilt is given as a screening marker for neurogenic OH.
• Causes span immobility, hypovolaemia, a long drug list (antihypertensives, diuretics, vasodilators, antidepressants, antipsychotics, sedatives), neurodegenerative disease, low-output cardiac lesions, endocrine disease and baroreceptor damage.
• Management is non-pharmacological first (salt >10 g/day or urinary sodium >170 mmol, fluid 1.5–2.5 L/day, water bolus before standing, counter-manoeuvres, compression, head-up bed). Drugs: fludrocortisone 50 µg daily increasing to 300 µg; midodrine 2.5 mg BD–10 mg TDS (contraindicated in severe heart disease, AKI, urinary retention, phaeochromocytoma, thyrotoxicosis); pyridostigmine 30–60 mg BD/TDS.

Syncope

• Initial evaluation is history, examination, orthostatic BP and 12-lead ECG. The history is structured as 3Ps before (provokers, posture, prodrome), the event itself, and recovery.
• Short-term high-risk criteria are listed in full — abnormal ECG (ischaemia, VT, AF, BBB or IVCD ≥120 ms, LVH, Q waves, bradycardia <50, pre-excitation, long/short QT, Brugada pattern, ARVC features), syncope supine or on exertion, palpitations at the time, chest pain or breathlessness, and important comorbidity.
• Treatment of vasovagal syncope: hydration ± salt, trigger avoidance, isometric counter-manoeuvres at prodrome, reduce hypotensive drugs targeting SBP 140 mmHg (class IIa), fludrocortisone 50–300 µg, midodrine 2.5 mg BD–15 mg TDS, and dual-chamber pacing in selected cases (IIa/IIb).

Limitations of the document

• It is not a primary source and carries no grading. Almost no section states class of recommendation or level of evidence, so its statements cannot be weighed against trial evidence without going back to the underlying guideline it cites. The wiki cites it for protocol and dosing, not for evidential strength.
• Its reference base is dated. Sections cite the 2014 ACC/AHA perioperative guideline, the 2015 ESC endocarditis guideline, the 2017 ACC/AHA hypertension guideline, the 2018 ESC/ESH hypertension guideline, the 2018 EHRA DOAC guide, and the 2021 ESC and 2022 AHA heart failure guidelines. The 2022 ESC non-cardiac surgery guideline is the most recent guideline cited anywhere in the chapter.
• The heart failure section has been overtaken. Its four-category LVEF classification and its single natriuretic-peptide rule-out both predate the 2026 ESC guideline, and its HFpEF therapy list omits the 2026 MRA recommendation. It is cited here as a record of the AHA 2022 position and of local practice, not as current guidance.
• Locally specific and not portable. Doses, formularies, availability statements (andexanet alfa unavailable) and interventional thresholds reflect Hong Kong Hospital Authority practice in 2024–2026. They should not be transplanted to another system without checking the local formulary.
• Conversion fidelity. The PDF was converted to markdown automatically. Heading structure was largely destroyed (6 H1s against 982 H6s), several clinical algorithms survive only as extracted image text, and some tables are imperfectly reconstructed. Doses and energies were cross-checked against the running prose where both existed; figures that exist only in images could not be verified.
• No dates on individual statements. The handbook does not mark which sections were revised in this edition beyond noting that rehabilitation and dermatology are new.

Key Concepts Mentioned

concepts/Cardiopulmonary-Resuscitation, concepts/Acute-Aortic-Syndrome, concepts/Cardiac-Tamponade, concepts/Decompensated-HF-Management, concepts/Hypertensive-Crisis, concepts/Infective-Endocarditis, concepts/Perioperative-Cardiovascular-Assessment, concepts/NOAC-Perioperative, concepts/Orthostatic-Hypotension, concepts/Syncope, entities/Acute-Coronary-Syndrome, entities/Heart-Failure, entities/Pulmonary-Embolism

Key Entities Mentioned

entities/Heart-Failure, entities/HFrEF, entities/HFpEF, entities/Acute-Coronary-Syndrome, entities/Pulmonary-Embolism, entities/Hypertension, entities/Atrial-Fibrillation, entities/Finerenone, entities/Sacubitril-Valsartan

Wiki Pages Updated

• wiki/sources/Handbook-HA-2024.md
• wiki/concepts/Cardiopulmonary-Resuscitation.md
• wiki/concepts/Acute-Aortic-Syndrome.md
• wiki/concepts/Cardiac-Tamponade.md
• wiki/concepts/Acute-Pulmonary-Oedema.md
• wiki/concepts/Hypertensive-Crisis.md
• wiki/concepts/Infective-Endocarditis.md
• wiki/concepts/Perioperative-Cardiovascular-Assessment.md
• wiki/concepts/NOAC-Perioperative.md
• wiki/concepts/Orthostatic-Hypotension.md
• wiki/concepts/Syncope.md
• wiki/entities/Heart-Failure.md
• wiki/entities/HFrEF.md
• wiki/entities/HFpEF.md
• wiki/entities/Acute-Coronary-Syndrome.md
• wiki/entities/Pulmonary-Embolism.md
• wiki/entities/Hypertension.md
• wiki/sourceindex.md
• wiki/wikiindex.md