• HF affects approximately 1–2% of the adult population worldwide, rising to > 10% in those aged > 70 years.
• In Hong Kong, the ageing population, high prevalence of hypertension (HT), diabetes mellitus (DM), and ischaemic heart disease (IHD) make HF a major public health burden.
• HFpEF is increasingly recognised and now accounts for roughly 50% of HF hospital admissions globally — this proportion is growing as the population ages and hypertension/obesity prevalence rises.
• HF is the leading cause of hospital admission in patients > 65 years.
• The 5-year mortality of HF remains approximately 50%, comparable to many cancers, underscoring its severity.

• IHD and hypertension are the leading causes of HF in Hong Kong (similar to Western data).
• Rheumatic heart disease, once a dominant cause, has declined markedly but still appears occasionally (especially in older patients or immigrants from mainland China/Southeast Asia).
• Hepatitis B-related cirrhotic cardiomyopathy and thalassaemia-related iron overload cardiomyopathy are locally relevant causes to keep in mind.

The heart is a dual pump in series:

• Right heart (RA → RV → pulmonary artery): receives systemic venous return and pumps to the lungs (low-pressure circuit, ~25/10 mmHg)
• Left heart (LA → LV → aorta): receives pulmonary venous return and pumps to the systemic circulation (high-pressure circuit, ~120/80 mmHg)

The LV is the workhorse — thick-walled (~1 cm), conical. The RV is thinner (~3–5 mm), crescent-shaped, designed for low-pressure work.

Key structures relevant to HF:

• Coronary arteries: supply the myocardium; obstruction → ischaemia → contractile failure
• Cardiac valves: ensure unidirectional flow; stenosis or regurgitation → pressure or volume overload
• Myocardium: composed of cardiomyocytes with intercalated discs (gap junctions for synchronous contraction)
• Conduction system: SA node → AV node → Bundle of His → bundle branches → Purkinje fibres; dysfunction → arrhythmias → ↓CO

$\text{Cardiac Output (CO)} = \text{Heart Rate (HR)} \times \text{Stroke Volume (SV)}$

Stroke volume is determined by:

1. Preload — the volume of blood in the ventricle at end-diastole (governed by Frank–Starling mechanism: ↑preload → ↑stretch → ↑contractile force, up to a point)
2. Afterload — the resistance the ventricle must overcome to eject blood (approximated by systemic vascular resistance for LV, pulmonary vascular resistance for RV)
3. Contractility (inotropy) — the intrinsic force of contraction independent of preload and afterload

$\text{Blood Pressure} = \text{CO} \times \text{SVR}$

"V = IR → Blood Pressure = CO × Peripheral Resistance → all drugs manipulate this equation." ^[7]

In health, cardiac output is tightly matched to metabolic demand via:

• Sympathetic nervous system (SNS): ↑HR (chronotropy), ↑contractility (inotropy), ↑SVR (vasoconstriction)
• Renin-angiotensin-aldosterone system (RAAS): salt/water retention → ↑preload; angiotensin II → vasoconstriction → ↑afterload
• Natriuretic peptides (ANP, BNP): released in response to myocardial stretch → promote natriuresis, diuresis, vasodilation — a counter-regulatory mechanism
• Antidiuretic hormone (ADH/vasopressin): water retention → ↑preload

In HF, the SNS and RAAS become chronically activated as compensatory mechanisms, but they ultimately become maladaptive — this is the central concept behind modern HF pharmacotherapy.

Think of it as: What has gone wrong with the pump, the plumbing, or the electrical system?

The major aetiological categories are:

Whatever the aetiology, the final common pathway is:

↓ Cardiac Output (or ↑ requirement the heart cannot meet) → Neurohormonal Activation → Maladaptive Remodelling → Progressive HF

This is the structural consequence of the chronic neurohormonal overdrive:

• Eccentric hypertrophy (volume overload, e.g., MR, DCMP): sarcomeres added in series → chamber dilatation, ↑wall stress
• Concentric hypertrophy (pressure overload, e.g., AS, HT): sarcomeres added in parallel → ↑wall thickness, ↓chamber compliance
• Remodelling involves: myocyte hypertrophy, myocyte apoptosis, interstitial fibrosis, changes in extracellular matrix
• Eventually → adverse remodelling: further dilatation, spherical shape change, functional MR (annular dilatation), ↓LVEF

Note: Both ultimately lead to elevated filling pressures → congestion. The difference is the mechanism, not the symptoms.

• Chronic LHF → ↑LA pressure → ↑pulmonary venous pressure → pulmonary hypertension (post-capillary, Group 2) → ↑RV afterload → RV dilation and failure
• This is why chronic left HF eventually leads to biventricular failure ^[6]

In reality, both coexist — but the concept helps you understand why some patients present with predominantly congestive symptoms and others with predominantly low-output symptoms.

Classification of HF by LVEF (GC lecture slide — HIGH YIELD): ^[1]

NYHA Classification (GC lecture slide — HIGH YIELD): ^[2]

The NYHA class is a subjective, functional assessment. It can change over time (improve with treatment or worsen with decompensation). It is used for:

• Communicating functional status
• Guiding therapy (e.g., certain devices are indicated in NYHA II–III)
• Prognostication

ACCF/AHA Staging (from lecture and senior notes): ^[2]

Key difference: NYHA class can go up and down (reversible), but ACC/AHA stages only progress forward (irreversible — once you have structural disease, you can't un-have it). This is why they complement each other.

Classification of HF by laterality: ^[6]

• Left HF (more common) → ↓LV CO
  • Acute → acute pulmonary oedema (APO)
  • Chronic → pulmonary congestion → eventually biventricular failure
• Right HF → ↓RV CO and ↑RA filling pressure → systemic venous congestion
• Biventricular HF due to:
  • Diffuse disease processes, e.g., DCMP, extensive IHD
  • Chronic left HF leading to right heart failure ^[6]

Classification of HF by cardiac output: ^[6]

• Acute HF (AHF): rapid onset or worsening of symptoms requiring urgent therapy (includes de novo AHF and acute decompensation of chronic HF [ADHF])
• Chronic HF (CHF): stable, persistent HF with ongoing symptoms managed with maintenance therapy

The clinical features of HF arise from two fundamental mechanisms:

1. Backward failure = congestion (fluid backs up behind the failing ventricle)
2. Forward failure = inadequate cardiac output (tissues don't receive enough perfusion)

Additionally, compensatory mechanisms (tachycardia, cardiomegaly) produce their own signs.

From GC lecture slides and senior notes: ^[6]

ECG features of HF include: ^[9]

• Poor R wave progression (reversed R wave, e.g., V2 bigger than V3, or V4 greater)
• Low voltage (highlights underlying cardiomyopathy)
• P pulmonale, P mitrale → atrial dilatation
• Ventricular hypertrophy

Other ECG findings to look for:

• Pathological Q waves → prior MI (ischaemic aetiology)
• Left bundle branch block (LBBB) → common in DCMP; also relevant for CRT eligibility
• Atrial fibrillation → both a cause and consequence of HF
• ST/T wave changes → ischaemia, LV strain pattern

The CXR is the quickest bedside tool for assessing pulmonary congestion. The mnemonic ABCDE is useful:

Additional:

• Cephalization = upper lobe pulmonary venous diversion (same as D above)
• Peribronchial cuffing = thickened, oedematous bronchial walls (seen on CXR as hazy rings around bronchi)

On history and physical examination: ^[10]

• SOB on exertion: sensitivity 66%
• Orthopnoea, PND and oedema: specificity 80%
• Tachycardia, basal crackles, ankle oedema, S3 gallop, neck vein distension: all have specificity over 90%
• "Not much sensitive, but there are some pretty specific findings"

This is why HF remains a clinical diagnosis supported by investigations — no single symptom or sign is both sensitive and specific enough to make the diagnosis alone. This is why the Framingham Criteria and BNP levels are important adjuncts.

When HF progresses to the point of end-organ hypoperfusion:

Clinical features of cardiogenic shock: ^[12]

• Forward failure: pallor, peripheral cyanosis, cold extremities, delayed capillary refill, oliguria, altered consciousness
• Backward failure: dyspnoea, wheeze, cough with pink frothy sputum, cyanosis, basal crackles, displaced apex, gallop

Every major HF drug targets the maladaptive compensatory mechanisms:

• ACEi/ARB/ARNI → block RAAS
• Beta-blockers → block SNS
• Mineralocorticoid receptor antagonists (MRA) → block aldosterone
• SGLT2 inhibitors → natriuresis, ↓preload, ↓inflammation (mechanism still being elucidated)
• Diuretics → ↓preload (volume reduction)
• Vasodilators → ↓afterload (hydralazine + isosorbide dinitrate)

Think systematically using organ systems:

PND and orthopnoea are the most important symptoms suggestive of cardiac-origin dyspnoea. ^[9][17] Their presence significantly raises the pre-test probability of HF over respiratory or other causes.

From senior notes (Felix PY Lai) — HIGH YIELD aetiological table: ^[2]

Cor pulmonale = RV failure due to respiratory disease (usually chronic). Requires pulmonary hypertension due to polycythaemia + hypoxic vasoconstriction → ↑PVR. ↑RV workload → RV failure. Often manifests during acute exacerbation. ^[21]

There is no single blood test, imaging finding, or biopsy result that defines heart failure. HF is a syndrome — a constellation of symptoms, signs, and objective evidence of cardiac dysfunction. This means diagnosis relies on pattern recognition at the bedside, supported by investigations. The investigations serve two roles: (1) confirm the clinical suspicion, and (2) identify the aetiology so you can treat the cause.

Heart failure is a clinical diagnosis. ^[10] It requires the simultaneous presence of: (1) symptoms or signs, (2) structural or functional cardiac abnormality, and (3) elevated intracardiac pressures or inadequate cardiac output. ^[4]

Heart failure is a clinical diagnosis → using the Framingham Criteria. Requires the simultaneous presence of at least 2 major criteria, or 1 major criterion in conjunction with 2 minor criteria. ^[1][10]

This is the classic bedside diagnostic tool. It was developed from the Framingham Heart Study — a long-running epidemiological cohort. The criteria are divided into major and minor based on their specificity for HF.

Logic behind the split: Major criteria are highly specific for HF (when present, they strongly suggest HF). Minor criteria are less specific — they can be caused by many non-cardiac conditions (e.g., ankle oedema from venous stasis, hepatomegaly from liver disease). That's why you need two minor criteria to match the diagnostic weight of one major criterion.

Rule: ≥ 2 major OR 1 major + 2 minor = diagnosis of HF

On the Moodle slides there is also a mention of the Boston classification, which seems even better for older community dwellers. ^[10] The Boston criteria incorporate history, physical examination, and CXR findings into a scoring system (max 12 points; ≥ 8 = definite HF, 5–7 = possible HF, ≤ 4 = unlikely HF). For exams, Framingham is the primary one to know.

Once HF is diagnosed, you need to classify how severe it is and what stage the disease is at. These have been covered in detail in Part 1 but are re-emphasised here as they form part of the diagnostic framework:

• NYHA Functional Class (I–IV): subjective, functional, reversible — tells you how symptomatic the patient is right now
• ACC/AHA Stage (A–D): structural, progressive, irreversible — tells you where the patient is on the disease trajectory
• Killip class: predicts mortality in post-MI heart failure ^[20]:
  • Class I: no clinical signs of HF
  • Class II: lung creps, S3 gallop, elevated JVP
  • Class III: frank APO (acute pulmonary oedema)
  • Class IV: cardiogenic shock (SBP < 90), peripheral vasoconstriction (oliguria, cyanosis, sweating) ^[20]

The Killip classification is specifically used in the post-MI setting — it was designed to estimate in-hospital mortality after acute MI based on the degree of heart failure. Higher Killip class = worse prognosis.

• Ross classification: for paediatric heart failure severity ^[5] — analogous to NYHA but adapted for children, incorporating feeding difficulty, diaphoresis, and tachypnoea

This is the GC 084 lecture algorithm — treat as highest-yield for in-house exams. ^[1]

The algorithm follows a logical step-wise approach: clinical suspicion → biomarkers → imaging → confirmation → treat by aetiology and stage.

Step-by-Step Walkthrough

Step 1: Initial Assessment of patients with suspected or possible heart failure ^[1]

Assess:

1. Symptoms — e.g., shortness of breath on effort, orthopnoea, PND
2. Past illness and baseline characteristics — hypertension, DM, history of CAD, use of cardiotoxic drugs, history of radiotherapy, history of diuretic therapy
3. Family history of cardiac disease — e.g., genetic disorders
4. Signs (including pulse oximetry) — rales, leg oedema, heart murmur, extra heart sounds (III, IV), jugular venous distension
5. ECG
6. Chest X-ray

If NONE of the above are present → HF is unlikely → Prevent HF or follow-up ^[1]

If one or more are present → proceed to Step 2 ^[1]

Step 2: Biomarker assessment ^[1]

NT-proBNP ≥ 400 pg/mL or BNP ≥ 100 pg/mL → proceed to echocardiography ^[1]

If BNP < 100 or NT-proBNP < 400 → HF is unlikely ^[1]

Step 3: Echocardiography (including stress echocardiography) ^[1]

• If echo is normal and no further evaluation indicated → HF is unlikely ^[1]
• If echo is abnormal or further evaluation is indicated → proceed to Step 4

Step 4: Advanced imaging / haemodynamic assessment ^[1]

CT, MRI, nuclear cardiology (exercise/pharmacological stress testing), or cardiac catheterisation ^[1]

Step 5: Confirmation and treatment ^[1]

Abnormal findings (+) → HF is confirmed → Treatment according to etiology and stage of HF ^[1]

Echocardiography is the essential investigation — it looks for the underlying cause and evaluates LVEF. LVEF alone is not diagnostic of HF. ^[6]

Echocardiography is the single most informative test in HF. It answers three fundamental questions:

1. Is there structural/functional abnormality? (confirms HF)
2. What is the LVEF? (classifies HFrEF vs HFmrEF vs HFpEF)
3. What is the cause? (valvular, ischaemic, cardiomyopathy, pericardial)

For DCM patients presenting with HF: ECG and CXR done first → then follow up with BNP/NT-proBNP → if BNP above cutoff range, indicates fluid overload and damage → echocardiogram to check EF, structural heart disease, regional wall motion abnormalities. For those without NT-proBNP, go directly to echo. ^[6]

Stress echocardiography (exercise or pharmacological with dobutamine): used when resting echo is inconclusive — can unmask inducible ischaemia or exercise-induced diastolic dysfunction (relevant for HFpEF diagnosis).

Once HF is confirmed, the investigation strategy should be directed at finding the cause. The table below summarises how different investigations help narrow the aetiology:

A frequently examined topic tying cardiology to hepatology:

Congestive heart failure causes an AST > ALT pattern on LFT. Other investigations: clinical information + ultrasound liver showing enlarged liver and engorged hepatic veins. ^[25]

There are only four liver pathologies with AST > ALT:

1. Alcoholic hepatitis (AST:ALT > 2:1, AST almost never > 500)
2. Hepatocellular carcinoma
3. Congestive heart failure
4. Ischaemic hepatitis (profound shock, disproportionate ↑LDH) ^[25]

The reason AST > ALT in CHF: hepatic congestion causes zone 3 (centrilobular) hypoxic injury — mitochondrial damage releases AST preferentially (AST is a mitochondrial enzyme), while ALT is predominantly cytosolic.

Why? Chronic SNS activation → ↑HR, ↑contractility (short-term benefit), but long-term → β1-receptor downregulation, direct catecholamine toxicity, myocyte apoptosis, arrhythmogenesis. Beta-blockers block these harmful effects.

Beta-blockers: ↓contractility → ↓workload, ↓SN activation → ↓arrhythmias. ^[6] Indication: as initial treatment in patients with no evidence of fluid overload → titrated slowly upwards to avoid precipitating acute decompensation. ^[6]

Bisoprolol is more cardioselective than metoprolol → even in patients with asthma, can still try bisoprolol, won't affect airway. ^[7]

Why? Aldosterone — even with ACEi/ARB, there is "aldosterone escape" (aldosterone production via non-ACE pathways). Aldosterone promotes Na⁺/H₂O retention, K⁺/Mg²⁺ loss, myocardial fibrosis, and baroreceptor dysfunction. MRAs block all of these.

MRA: antagonises detrimental mineralocorticoid action. ^[6] Indications: as secondary therapy in those with NYHA II–IV and LVEF ≤ 35% on optimal therapy. ^[6] Benefit: demonstrated ↑survival in those with NYHA II–IV and LVEF ≤ 35%. ^[6]

Why? Originally an anti-diabetic drug, SGLT2i ("sodium-glucose co-transporter 2 inhibitor") has pleiotropic cardiovascular and renal benefits that go far beyond glucose-lowering:

• Osmotic diuresis + natriuresis → ↓preload (reduces congestion without activating RAAS as aggressively as loop diuretics)
• ↓Cardiac preload and afterload → ↓wall stress
• ↓Interstitial fibrosis and inflammation
• Metabolic effects: shifts myocardial fuel utilization towards ketone bodies (more efficient fuel for the failing heart)

SGLT2i is interesting since it's an antidiabetic → cardioprotective effects by diuresis. Very safe, rarely causes hypoglycaemia and hypotension. ^[7]

Why? Diuretics are the only drug class that can effectively relieve congestion (fluid overload). They have no mortality benefit but are essential for symptom control.

Diuretics indicated if volume overload → ↓preload due to ↓fluid retention → monitor RFT and body weight. ^[20]

S/E: dizziness, GI discomfort, nocturia, hypokalaemia (loop/thiazide). ^[20]

Diuretic resistance is a common problem in advanced HF. Strategies:

1. IV instead of oral (gut oedema may impair absorption)
2. Continuous infusion instead of bolus
3. Add thiazide (metolazone) to loop diuretic — "sequential nephron blockade"
4. Add acetazolamide (ADVOR trial — proximal tubule blockade)

Digoxin: positive inotropic agent — ↑contractility without ↑HR. ^[20] Indication: patients with AF; persistent symptoms despite treatment. ^[20] Narrow therapeutic index → TDM 8h post-dose. S/E: dizziness, N/V/D, arrhythmia. Renal excretion: affected by K⁺/Ca²⁺. ^[20]

• Digoxin inhibits the Na⁺/K⁺-ATPase → ↑intracellular Na⁺ → reverses Na⁺/Ca²⁺ exchanger → ↑intracellular Ca²⁺ → ↑contractility
• Also has vagotonic effect → slows AV conduction → useful for rate control in AF
• No mortality benefit, but reduces hospitalisation
• Toxicity enhanced by: hypokalaemia, hypomagnesaemia, hypercalcaemia, renal impairment, hypothyroidism

Digoxin: seldom used due to narrow therapeutic index. ^[5]

Nitrates/hydralazine: venous/coronary vasodilation (nitrates) + arterial vasodilation (hydralazine). ^[6] Indication: (1) alternative to ACEi/ARB (e.g., severe renal failure) as initial therapy; (2) secondary therapy in addition to ACEi/ARB + BB + MRA in Black individuals. ^[6] Benefit: ↓mortality in Black individuals with NYHA III–IV + LVEF ≤ 35%. ^[6]

The combination mimics the haemodynamic effects of ACEi/ARB (↓preload + ↓afterload) without affecting the kidneys or potassium.

Ivabradine: blocks HCN channel → pure ↓HR effect on heart → ↓cardiac workload. ^[6] Indication: secondary therapy for patients in sinus rhythm with HR > 70 bpm despite max BB and NYHA II–III + LVEF ≤ 35%. ^[6] Benefit: ↓mortality and ↓admission for above patients. ^[6]

• HCN = "hyperpolarisation-activated cyclic nucleotide-gated" channel = the "funny" (If) current in the SA node that controls pacemaker rate
• Ivabradine selectively slows the SA node without affecting contractility, AV conduction, or BP — a "pure chronotrope"
• Requires sinus rhythm (useless in AF — the ventricular rate in AF is not determined by the SA node)

Vericiguat: add-on drug for specific populations. ^[7]

• Soluble guanylate cyclase (sGC) stimulator → enhances NO-sGC-cGMP pathway → vasodilation
• Indicated in patients with worsening HFrEF despite optimal therapy (recent hospitalisation or IV diuretic use)
• Key trial: VICTORIA

The mnemonic "LMNOP" is classic:

For cardiogenic shock: optimise cardiac workload by inotropes (e.g., IV dobutamine) if adequate filling pressure; fluid resuscitation ± vasopressors if low filling pressure. ^[12]

Management of cardiogenic shock: ^[12]

1. Sit patient upright
2. High-flow O₂ (15 L/min) with BVM with reservoir to keep SpO₂ > 94%
3. Optimise cardiac workload:
   • Inotropes (e.g., IV dobutamine) if adequate filling pressure
   • Fluid resuscitation ± vasopressors if low filling pressure
4. Investigations and treatment for underlying cause concurrently:
   • RFT, ECG, CXR, ABG, cardiac enzymes, echocardiogram
5. ACLS if arrhythmogenic cause

Inotropes used in acute HF:

Always search for and treat the precipitant of acute decompensation. A useful mnemonic is "FAILURES":

• Forgot medications (non-compliance)
• Arrhythmia / Anaemia
• Ischaemia / Infection
• Lifestyle (dietary salt/fluid excess)
• Upward titration problems (of HF meds)
• Renal failure
• Embolism (PE)
• Stenosis (new or worsening valvular disease)

Why? In patients with LBBB, the LV septum and lateral wall contract asynchronously → ↓EF. CRT involves pacing both ventricles simultaneously to restore synchrony.

CRT (biventricular pacing) should be considered for patients with ALL of the following: ^[10]

• NYHA III despite optimal medical therapy
• Sinus rhythm
• Widened QRS ( > 120 ms) → left bundle branch block
• LVEF < 35% and LVD > 5.5 cm

LBBB → septum contracts, then lateral wall contracts, then septum contracts again → walls not contracting synchronously → reduced EF → can be amenable by CRT. ^[4]

Data shows more beneficial for LBBB patients, but not RBBB patients → which is why guidelines still recommend for LBBB. ^[10]

Why? Patients with severely reduced LVEF are at high risk of sudden cardiac death from ventricular arrhythmias (VT/VF). An ICD detects and terminates these arrhythmias.

Primary prevention ICD: should be considered in patients with NYHA II–III (LVEF < 30%), may be considered if LVEF 31–35%. ^[10]

• Following 3 months of optimal medical therapy in patients with PMH of MI (ischaemic)
• Following 6 months of optimal medical therapy in non-ischaemic patients ^[10]

Secondary prevention: in patients who have already had an episode of VT/VF. ^[10]

The rationale for waiting 3–6 months: optimal medical therapy (especially BB, ARNI, SGLT2i) may improve LVEF above the ICD threshold, avoiding an unnecessary device.

ICD: prevention of arrhythmias if LVEF < 35% or Hx of VT/VF. ^[20]

CABG: ischaemic cardiomyopathy ^[10] — revascularisation may improve LV function if there is viable but hibernating myocardium (demonstrated by viability studies such as MRI, PET, or dobutamine stress echo).

Mechanical circulatory support (e.g., IABP, LVAD, ECMO) for potentially reversible pump dysfunction. Indications: myocarditis, post-cardiopulmonary bypass myocardial dysfunction. ^[5]

LVAD / Heart transplant → for intractable ventricular arrhythmias / heart failure. ^[6]

Cardiac transplantation: refractory heart failure. ^[10]

Common indications in HK: idiopathic DCMP (commonest), ischaemic heart disease (2nd commonest), valvular heart disease, congenital heart disease (post-ToF, post-Fontan, HOCM). ^[6]

• Mechanism: LV dilatation → mitral annular dilatation → leaflets fail to coapt → regurgitation through a structurally normal valve. Similarly, RV dilatation → tricuspid annular dilatation → functional TR.
• This creates a vicious cycle: MR → more volume overload on LV → more dilatation → worse MR

Complications of IHD include: heart failure, arrhythmias, VSD (anterior septal wall MI), mitral regurgitation complicating papillary muscle dysfunction (inferior MI). ^[29]

• In acute MI, papillary muscle ischaemia or rupture can cause acute severe MR → flash pulmonary oedema
• Functional MR and poor LV → refractory HF ^[30]

• Ongoing neurohormonal activation → myocyte hypertrophy, apoptosis, and fibrosis → adverse remodelling
• LV becomes more spherical → further worsens functional MR → further ↓CO
• Eventually leads to end-stage HF (NYHA IV, ACC/AHA Stage D) requiring advanced therapies

• Mechanism: LHF → ↑LVEDP → ↑LA pressure → ↑pulmonary venous pressure → fluid transudation into interstitium then alveoli
• Acute pulmonary oedema (APO): medical emergency — pink frothy sputum, severe dyspnoea, crepitations extending from bases to apices, SpO₂ dropping
• Chronic pulmonary congestion: progressive SOBOE, PND, orthopnoea, nocturnal cough
• Corresponds to Killip Class III (frank APO) or Class IV (cardiogenic shock) in the post-MI setting ^[20]

• Mechanism: Chronic ↑LA pressure → passive transmission to pulmonary vasculature → ↑pulmonary venous pressure → eventually reactive pulmonary arteriolar vasoconstriction and remodelling → combined pre- and post-capillary PH
• Haemodynamic definition: mPAP > 20 mmHg with PAWP > 15 mmHg
• Consequences: ↑RV afterload → RV dilatation and failure → progression from isolated LHF to biventricular failure
• If fixed pulmonary HTN unresponsive to drugs develops, it becomes a contraindication to cardiac transplantation (the donor RV cannot cope with high PVR) ^[6]

• Pulmonary congestion creates a favourable environment for lower respiratory tract infections
• Impaired mucociliary clearance, interstitial oedema, poor cough reflex (especially in elderly/frail)
• Infections in turn precipitate acute decompensation (fever → ↑metabolic demand → ↑HR → ↓diastolic filling)

• Transudative effusions from ↑capillary hydrostatic pressure (both pulmonary and systemic venous pathways drain the pleura)
• Typically bilateral, or right-sided if unilateral (right hemidiaphragm is lower, more pleural surface)
• Contributes to dyspnoea via lung compression and atelectasis

• Mechanism: ↓CO → ↓renal perfusion → ↓GFR (pre-renal AKI). Chronic renal hypoperfusion + venous congestion (↑renal venous pressure from RHF) → tubulointerstitial fibrosis → CKD
• Neurohormonal activation (RAAS, SNS) → renal vasoconstriction → further ↓GFR
• Heart failure is a recognised risk factor for developing AKI ^[31]

The cardiorenal syndrome describes the bidirectional relationship:

• Type 1: Acute HF → acute AKI
• Type 2: Chronic HF → progressive CKD
• Type 3: Acute kidney disease → acute HF
• Type 4: CKD → chronic HF
• Type 5: Systemic disease affecting both (e.g., DM, amyloidosis, sepsis)

• Chronic HF + CKD → ↓diuretic delivery to tubules → ↓response to loop diuretics
• Gut oedema → ↓oral absorption of diuretics
• Management: IV diuretics, sequential nephron blockade (add thiazide), ultrafiltration in refractory cases

• Mechanism: RHF → ↑RA pressure → ↑hepatic venous pressure → hepatic sinusoidal distension → tender hepatomegaly
• If significant TR, the liver may be pulsatile ^[6] — systolic regurgitant jet transmits retrograde through hepatic veins
• LFT pattern: AST > ALT in congestive heart failure ^[25] — centrilobular (zone 3) hypoxic injury releases mitochondrial AST preferentially; ↑GGT > 2× ULN ^[2]

• Chronic, longstanding RHF → persistent centrilobular necrosis and fibrosis → "nutmeg liver" (mottled appearance on cross-section: congested centrilobular zones alternating with paler periportal zones) → eventual cirrhosis
• Rare in modern practice (effective diuretics and HF treatment prevent this progression)
• Complications of cardiac cirrhosis mirror those of other forms of cirrhosis: ascites, coagulopathy, portal hypertension

Cardiac failure is listed as a post-hepatic cause of portal hypertension ^[32]

• Occurs in acute cardiogenic shock or severe low-output states
• Dramatic, sudden rise in transaminases (often > 1000 IU/L), with AST > ALT and disproportionate ↑LDH
• Resolves when haemodynamics are restored — the liver has excellent regenerative capacity if the insult is brief

HF fulfils all three components of Virchow's triad:

1. Stasis: ↓CO → sluggish blood flow, especially in dilated cardiac chambers
2. Endothelial injury/dysfunction: chronic neurohormonal activation, inflammation
3. Hypercoagulability: upregulated coagulation factors, ↑platelet activation

Complications of valvular disease include: thromboembolism (turbulent flow), infective endocarditis, and problems during pregnancy. ^[30][33]

• Anticoagulation: Always indicated if concurrent AF (warfarin or DOAC depending on valve status — MS requires warfarin, not DOAC ^[28]); consider if LV thrombus detected; prophylactic LMWH during hospitalisation for all immobilised HF patients

• Definition: Unintentional weight loss > 5% of body weight over 6–12 months in a patient with HF
• Mechanism: Multifactorial —
  1. Anorexia and ↓absorption (due to GI congestion) ^[6]
  2. Poor tissue perfusion ^[6]
  3. Skeletal muscle atrophy (due to immobility) ^[6]
  4. Pro-inflammatory cytokines (TNF-α, IL-1, IL-6) → catabolic state → muscle wasting
  5. Neurohormonal activation → increased basal metabolic rate
• Significance: Cardiac cachexia is an independent predictor of mortality in HF. It signals advanced, refractory disease.
• Management: Nutritional support, exercise rehabilitation, omega-3 fatty acids (modest evidence), treat underlying HF aggressively

• Very common in HF (up to 50% of patients), even without anaemia
• Mechanism: chronic inflammation → ↑hepcidin → ↓iron absorption and release from stores; GI congestion → ↓absorption; some renal iron loss
• Consequences: worsens exercise capacity, fatigue, and dyspnoea independent of Hb level
• Management: IV ferric carboxymaltose (FAIR-HF, AFFIRM-AHF trials) — improves symptoms, exercise capacity, and quality of life

• Multifactorial: iron deficiency, CKD (↓EPO), haemodilution, chronic disease, ACEi (↓EPO release)
• Worsens HF by reducing O₂-carrying capacity → compensatory ↑CO → further burden on failing heart
• Anaemia can exacerbate HF ^[2]

• Covered in Section 3.3 above
• Indicator of severe HF ^[2] — Na⁺ < 135 mmol/L in HF correlates with ↑mortality
• Due to non-osmotic ADH release → free water retention exceeds sodium retention

• Mechanism: ↓renal perfusion → ↓uric acid excretion; loop diuretics compete with uric acid for secretion in the proximal tubule → ↓urate clearance → hyperuricaemia → gout
• Furosemide-induced hyperuricaemia is a very common exam scenario

• In cardiogenic shock or severe low-output state → tissue hypoperfusion → anaerobic metabolism → lactic acidosis
• Lactate > 2 mmol/L is a marker of tissue hypoperfusion and poor prognosis

• ↓CO → ↓cerebral blood flow → cognitive impairment, confusion, syncope/pre-syncope
• Chronic low-grade cerebral hypoperfusion may contribute to vascular dementia

• Mechanism: Prolonged circulation time (due to ↓CO) → delayed feedback from central chemoreceptors → oscillating respiratory drive → cyclical crescendo-decrescendo breathing with intervening apnoea
• Very common in advanced HF (30–40% of patients with NYHA III–IV)
• Leads to: nocturnal hypoxaemia, sleep fragmentation, sympathetic activation → worsens HF
• Treatment: optimise HF therapy; adaptive servo-ventilation (ASV) — but SERVE-HF trial showed harm in HFrEF patients with predominant central sleep apnoea, so ASV is now contraindicated in HFrEF with LVEF ≤ 45%

• Prevalence: ~20–40% of HF patients
• Bidirectional relationship: depression → poor medication compliance, physical inactivity, SNS activation → worsens HF; HF → functional limitation, social isolation, poor prognosis → depression
• Screening and treatment (SSRIs preferred; avoid TCAs — anticholinergic effects, arrhythmia risk)

With our drugs nowadays, some patients who are originally HFrEF will become HFpEF → if 2 identical patients, one with HFrEF and one with HFpEF → the HFrEF will have higher mortality. But HFpEF patients are usually older with more comorbidities, so if you account for all other factors HFpEF may have worse prognosis. ^[10]

AOS Geriatrics: An 85-year-old woman with CHF + COPD, Clinical Frailty Scale 8 (very severe frailty), cachectic, minimally responsive → most appropriate management: focus on comfort measures and provide palliative care, respecting her dignity and preferences. ^[34]

When HF becomes refractory (Stage D) and the patient is not a candidate for transplant or LVAD:

• Shift focus from disease-modifying therapy to symptom management and quality of life
• Opioids for dyspnoea (low-dose morphine)
• Continue diuretics for comfort (reduce congestion)
• De-escalate medications that no longer provide benefit (e.g., statins, antidiabetics for tight control)
• Discuss goals of care, advance directives, and do-not-resuscitate orders
• Involve palliative care team early