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🫀 HKMLE MODULE 1B: HEART FAILURE

Ace-Level Comprehensive Study Note

Sources: Braunwald's Heart Disease 12e | Goldman-Cecil Medicine | Fuster & Hurst's The Heart 15e | Goodman & Gilman's Pharmacological Basis | Tintinalli's Emergency Medicine | 2022 AHA/ACC/HFSA Guidelines | HA QEH CHF Programme Report (Sept 2024) | PubMed landmark trials

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📌 QUICK SUMMARY

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1. DEFINITION

• Acute HF (AHF): New-onset or rapid deterioration of HF requiring urgent hospitalisation
• Chronic HF (CHF): Stable, long-standing HF managed in outpatient setting
• Acute decompensated HF (ADHF): Acute worsening of previously stable chronic HF

Do NOT confuse: Asymptomatic LV dysfunction (abnormal echo but no symptoms) = Stage B, not yet HF. This matters for management choices.

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2. CLASSIFICATION

2A. ACC/AHA Staging (Progressive, cannot go backwards)

2B. NYHA Functional Classification (Can fluctuate)

2C. EF-Based Classification (2022 AHA/ACC/HFSA)

2D. Haemodynamic Classification (Clinical Bedside)

2E. Acute HF Phenotypes (Tintinalli / ESC)

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3. AETIOLOGY / CAUSES

Mnemonic: "I HAVE CADS" (causes of HF)

• In HK/Chinese populations, non-ischaemic dilated cardiomyopathy is proportionally more common than in Western series
• Hypertension is the dominant cause of HFpEF in Chinese patients
• Tachycardia-induced cardiomyopathy from untreated AF is clinically significant (and reversible!)
• Cardiac amyloidosis (TTR type) is increasingly recognised - new 2022 guidelines have dedicated screening recommendations

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4. PATHOPHYSIOLOGY

Step-by-Step (Beginner-Friendly)

STEP 1 - Initial cardiac injury (MI, hypertension, valve disease, etc.)
         ↓
STEP 2 - ↓ Cardiac output → ↓ renal perfusion
         ↓
STEP 3 - NEUROHORMONAL ACTIVATION:
         → SNS activation: ↑HR, ↑contractility (short-term good, long-term bad)
         → RAAS activation: Angiotensin II → vasoconstriction, aldosterone → Na/water retention
         → ADH (vasopressin) release → water retention
         ↓
STEP 4 - MALADAPTIVE REMODELLING:
         → Ventricular dilation & hypertrophy (eccentric in HFrEF, concentric in HFpEF)
         → Fibrosis, cardiomyocyte apoptosis
         → β-receptor downregulation (blunts catecholamine response)
         ↓
STEP 5 - CONGESTION (backward failure):
         → LV failure → ↑LVEDP → ↑LA pressure → pulmonary congestion → dyspnoea
         → RV failure → ↑RV pressure → systemic venous congestion → oedema, ascites
         ↓
STEP 6 - LOW OUTPUT (forward failure):
         → ↓CO → fatigue, ↓renal perfusion (cardiorenal syndrome), ↓cerebral perfusion

HFrEF vs HFpEF Pathophysiology

• Neprilysin degrades BNP and other vasoactive peptides. Sacubitril inhibits neprilysin, so after starting sacubitril/valsartan (ARNI), BNP rises (not a sign of worsening!) but NT-proBNP falls. Use NT-proBNP to monitor, not BNP, in patients on ARNIs. - Goodman & Gilman's, p.670
• Beta-blockers work paradoxically: they reduce EF acutely but over 3-6 months produce a paradoxical increase in LVEF by reversing the HF gene programme (downregulation of beta-receptor density, improved SR Ca²+ handling, reduced arrhythmia propensity) - Goodman & Gilman's, p.670

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5. RISK FACTORS

Mnemonic: "HF DOCS"

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6. SYMPTOMS

Mnemonic: "FORD PO" (Fluid Overloaded Reduced Dyspnoeic Patient Originally)

• Acute-onset severe dyspnoea at rest
• SaO2 <90% on air
• SBP <90 mmHg (shock)
• New or worsening chest pain (ACS precipitant)
• Syncope or pre-syncope
• Rapid weight gain >2 kg in 24-48 hours
• Anuria or severe oliguria

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7. SIGNS

Mnemonic: "JVP RULES" (Jugular, Vascular, Peripheral, Respiratory, Underfilled/Liver, ECG changes... Sounds)

1. General: Dyspnoea at rest? Oxygen? Cachexia? Malar flush (MS)?
2. Hands: peripheral cyanosis, clubbing (unusual in HF alone - think other causes), capillary refill, pulse (rate, rhythm, character - pulsus alternans in severe HF)
3. Face: pallor, jaundice, malar flush
4. JVP: Patient at 45°, measure in cm above sternal angle. Confirm - press liver (HJR test)
5. Apex beat: Locate by palpation. Note position, character (heaving/thrusting)
6. Auscultation: Added sounds (S3 = volume overload = bad; S4 = pressure overload), murmurs (cause or complication)
7. Lungs: bibasal crepitations (fine = pulmonary oedema; coarse = infection)
8. Abdomen: liver size, tenderness, pulsatility; ascites (shifting dullness, fluid thrill)
9. Legs: pitting oedema up to which level? (ankle / knee / thigh / sacrum)

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8. INVESTIGATIONS

Mnemonic: "BENCH" (Bedside - ECG - Natriuretic peptides - Chest X-ray - Heart echo)

Diagnostic Algorithm: Bedside → Labs → Imaging → Functional

BEDSIDE

LABS

IMAGING

FUNCTIONAL

• Result: CTR 0.55, bilateral perihilar haziness, upper lobe diversion, Kerley B lines, right pleural effusion
• Interpretation: "Cardiomegaly with features of moderate-severe pulmonary oedema and right-sided pleural effusion consistent with decompensated left heart failure"

• BNP = 850 pg/mL (on ARNI), NT-proBNP = 3200 pg/mL
• Interpretation: "Elevated NT-proBNP consistent with decompensated HF. Note: BNP may be falsely elevated in ARNI patients (neprilysin inhibition raises BNP); use NT-proBNP for monitoring instead"

• Rate 95 bpm, AF, QRS 145ms, LBBB morphology
• Interpretation: "AF with broad complex LBBB - QRS >130ms LBBB pattern = CRT candidate if EF ≤35%"

• pH 7.32, pO2 58, pCO2 32, HCO3 16, lactate 3.2
• Interpretation: "Type 1 respiratory failure with metabolic acidosis and elevated lactate - signifies severe acute pulmonary oedema with early cardiogenic shock; start CPAP, IV diuretics, consider intubation if deteriorating"

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9. MANAGEMENT

9A. ACUTE MANAGEMENT - Acute Pulmonary Oedema (APO)

Emergency Verbal Orders (OSCE Script):

"I would immediately:
1. SIT the patient upright (reduces venous return, ↓preload)
2. Give HIGH-FLOW OXYGEN 15L/min via non-rebreather mask
   (or CPAP if SaO2 remains <90% - first-line NIV in APO)
3. Attach cardiac monitor, pulse oximeter, IV access x2
4. Give IV FUROSEMIDE 40-80mg IV bolus (or 2.5x usual oral dose if already on diuretic)
5. IV MORPHINE 2.5-5mg (cautious - reduces anxiety, preload;
   CAUTION: may suppress respiratory drive)
6. IV GLYCERYL TRINITRATE (GTN) infusion 10-200 mcg/min if SBP >90 mmHg
   (reduces both preload AND afterload)
7. Bloods: ABG, FBC, U&E, troponin, BNP/NT-proBNP, TFT, glucose
8. ECG, portable CXR
9. If SBP <90 mmHg = CARDIOGENIC SHOCK → DO NOT give vasodilators;
   give DOBUTAMINE infusion, consider NORADRENALINE, call ICU"

Mnemonic for APO Management: "LMNOP"

9B. CARDIOGENIC SHOCK Management

• V - Vasopressors (Noradrenaline - first-line pressor)
• A - Adrenaline (for refractory shock)
• L - Levosimendan (calcium sensitiser - used in HK HA day admission; improves CO without ↑O2 demand)
• I - Inotropes: Dobutamine (first-line inotrope, β1 agonist - reduces PCWP, ↑CO)
• D - Diuretics (CAUTIOUS - may worsen hypotension in cold/dry profile L)
• C - Coronary revascularisation if ACS-related shock (primary PCI)
• A - IABP (Intra-aortic balloon pump) / ECMO / LVAD as bridge
• R - Reperfusion if ischaemic cause
• D - Diagnose and treat reversible cause (RV MI, tamponade, massive PE)

• Levosimendan is used at QEH and other HA hospitals as IV day-case treatment for decompensated HF not responding to diuretics
• Mechanism: calcium sensitiser + K-ATP channel opener → inotropy + vasodilation without increasing myocardial oxygen demand
• Given as a 24-hour infusion 0.05-0.2 mcg/kg/min
• NOT available in all hospitals; requires cardiology input
• NOT a substitute for GDMT - symptomatic bridge only

9C. CHRONIC HF MANAGEMENT - HFrEF (LVEF ≤40%)

The "FOUR PILLARS" of GDMT - Quadruple Therapy

┌─────────────────────────────────────────────────────────────────────┐
│                    HFrEF GDMT QUADRUPLE THERAPY                     │
│                                                                       │
│  Pillar 1: ACEi/ARB/ARNI (RAAS inhibitor)                           │
│  Pillar 2: Beta-blocker (evidence-based: bisoprolol, carvedilol,     │
│                          metoprolol succinate CR/XL)                 │
│  Pillar 3: MRA - Spironolactone or Eplerenone                       │
│  Pillar 4: SGLT2 inhibitor - Dapagliflozin or Empagliflozin        │
└─────────────────────────────────────────────────────────────────────┘

Pharmacology Table - HFrEF Drugs

• HA QEH Comprehensive HF Programme (2022-present): targets all 4 GDMT pillars from inpatient stay onward
• Drug of choice for ARNI in HK HA: Sacubitril/valsartan (Entresto) - approved on HA Drug Formulary
• Target: >80% of HF patients on all 4 pillars at 6 months (QEH achieved this with their programme)
• Nurse-led HF clinic for up-titration (transition clinic after discharge)
• IV iron supplementation offered as day-case procedure for iron-deficient HF patients

9D. CHRONIC HF MANAGEMENT - HFpEF (LVEF ≥50%)

9E. NON-PHARMACOLOGICAL MANAGEMENT

Lifestyle Modification - Mnemonic: "SWEDS"

9F. DEVICE THERAPY

ICD (Implantable Cardioverter Defibrillator)

• HFrEF with LVEF ≤35% despite ≥3 months optimal GDMT
• NYHA Class II-III
• Life expectancy >1 year

CRT (Cardiac Resynchronisation Therapy)

• LVEF ≤35%
• NYHA Class II-IV
• LBBB with QRS ≥150ms (Class 1A) OR QRS 120-149ms (Class 2a)
• Already on optimal GDMT

• ICD and CRT implantation performed at Queen Mary Hospital (QMH), Queen Elizabeth Hospital (QEH), Prince of Wales Hospital (PWH), and Pamela Youde Nethersole Eastern Hospital (PYNEH)
• Referral via specialist outpatient cardiology clinic (SOPC)
• Pre-procedure: Echo confirmation of LVEF, optimised GDMT for ≥3 months, informed consent

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10. COMPLICATIONS

Mnemonic: "ARCHERY" (Arrhythmia, Renal, Cachexia, Hepatic, Embolism, Respiratory, Ye olde sudden death)

Cardiorenal Syndrome (CRS) - Important Complication

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11. PROGNOSIS AND RISK STRATIFICATION

General Prognosis

• 5-year mortality after HF diagnosis: ~50% (comparable to many cancers)
• 1-year mortality after hospitalisation for HF: ~25%
• Median survival: ~5 years from diagnosis (NYHA III-IV: 1-2 years)

Poor Prognostic Factors - Mnemonic: "BAD HEART"

Risk Scoring Tools

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12. COUNSELLING SCRIPT

"Your tests show that your heart is not pumping as well as it should be. This is called heart failure - it does not mean your heart has stopped, but it means your heart muscle is weaker and has to work harder. Because of this, fluid builds up in your lungs (making you short of breath) and in your legs (causing swelling).

The good news is that there are very effective medicines that can help your heart work better, reduce your symptoms, and help you live longer. We will start you on several medications - each works in a different way to protect your heart.

You will need to: weigh yourself every morning before eating. If your weight goes up more than 2 kilograms in 2 days, please call us or come to A&E. Reduce salty foods - no added salt at the table. Take your medicines every day - do not stop them even if you feel well.

We will see you in clinic every few weeks at first to adjust your medicines. If you feel worse - more breathless, more swollen, or very dizzy - come to hospital straight away."

• Many Chinese patients associate "heart failure" with immediate imminent death - clarify it is a chronic manageable condition
• Emphasise medication adherence - "four types of medicine, each has a different job"
• Daily weight monitoring may be new concept - provide written action plan with threshold
• Some patients may prefer traditional Chinese medicine (TCM) - advise not to replace GDMT but inform your doctor of any herbal supplements (especially those containing liquorice which can worsen fluid retention and hypertension)

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13. LEGAL & ETHICAL ORDINANCES

• Heart failure is NOT a statutory notifiable disease in Hong Kong
• Advanced directive / Advanced care planning (ACP): Increasingly important in HF (progressive disease). Refer to HA ACP policy. Under HK law (Cap. 136 Mental Health Ordinance), decisions for incapacitated patients require consideration of best interests; HK does not yet have a statutory ADE (Advance Directive) law but recognises common law validity
• Driving: Advise patients with NYHA Class III-IV or recent syncopal/ICD shock to stop driving; notify Transport Department. Under HK Road Traffic Ordinance (Cap. 374), medical fitness is required for driving licence
• End-of-life in advanced HF (Stage D): Palliative approach, symptom management, ICD deactivation counselling - discuss with patients/families. ICD deactivation is ethically permissible and does NOT constitute euthanasia (withdrawal of life-sustaining treatment)
• Drug prescription safety: Prescribing SGLT2i off-label for HF in non-diabetic patients - now evidence-based per 2022 guidelines; document indication clearly in records

• Heart failure itself is NOT notifiable
• However, if HF is caused by Chagas disease (rare in HK but imported) - the underlying cause may have public health implications. Acute rheumatic fever (which can cause valvular HF) is also not notifiable in HK

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14. COMMON EXAM QUESTIONS

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15. TABLES

⚠️ DRUG TRAPS TABLE

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📊 NOTABLE TRIALS TABLE

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🧠 MASTER MNEMONICS TABLE

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🔗 CROSS-MODULE LINKS

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🔬 BASIC SCIENCE INTEGRATION (SUMMARY)

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🏢 HA CLINICAL PATHWAY SUMMARY

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Sources cited:

• Braunwald's Heart Disease 12e - Fuster & Hurst's The Heart 15e - Goldman-Cecil Medicine - Goodman & Gilman's Pharmacological Basis - Tintinalli's Emergency Medicine
• 2022 AHA/ACC/HFSA Heart Failure Guidelines (Heidenreich PA et al., Circulation 2022)
• HA QEH CHF Programme Report HAB-P355 (September 2024)
• PARADIGM-HF, DAPA-HF, EMPEROR-Reduced/Preserved, DELIVER, TRED-HF, MERIT-HF, CIBIS-II, RALES, EMPHASIS-HF landmark trials
• Vaduganathan M et al. SGLT-2 inhibitors in HF: comprehensive meta-analysis of 5 RCTs. Lancet 2022, PMID 36041474
• Jhund PS et al. Dapagliflozin across the range of ejection fraction. Nat Med 2022, PMID 36030328
• Anker SD et al. Empagliflozin in HFpEF (EMPEROR-Preserved). NEJM 2021, PMID 34449189