2.2 Heart Failure & Cardiogenic Shock

Heart Failure & Cardiogenic Shock

Heart failure is a complex clinical syndrome characterised by structural or functional impairment of ventricular filling or ejection, leading to elevated intracardiac pressures and inadequate cardiac output at rest or during exertion. In the UK, heart failure affects approximately 1 million individuals and accounts for 5% of all emergency hospital admissions. Clinical practice differentiates acute decompensated heart failure (ADHF), chronic heart failure across ejection fraction phenotypes, and catastrophic cardiogenic shock.

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1. Classification & Pathophysiology

Ejection Fraction Phenotypes

The European Society of Cardiology (ESC) and UK NICE guidelines categorize heart failure according to left ventricular ejection fraction (LVEF) on transthoracic echocardiography:

• HFrEF (Heart Failure with Reduced Ejection Fraction): LVEF ≤40%. Characterised by systolic pump failure, progressive left ventricular dilatation, and eccentric remodelling. Most evidence-based prognostic therapies specifically benefit this cohort.
• HFmrEF (Heart Failure with Mildly Reduced Ejection Fraction): LVEF 41–49%. Represents a transitional phenotype that frequently benefits from similar therapies to HFrEF.
• HFpEF (Heart Failure with Preserved Ejection Fraction): LVEF ≥50% with evidence of spontaneous or provokable elevated LV filling pressures (e.g. elevated natriuretic peptides, diastolic dysfunction on Doppler echo, left atrial enlargement). Common in elderly, hypertensive, and female patients.

Neurohormonal Maladaptation

Myocardial injury (from ischaemia, hypertension, cardiomyopathy, or myocarditis) leads to reduced cardiac output, triggering compensatory neurohormonal pathways:

1. Sympathetic Nervous System (SNS): Catecholamine release increases heart rate and contractility, but chronically induces myocyte apoptosis, downregulates beta-1 adrenergic receptors, and causes peripheral vasoconstriction.
2. Renin-Angiotensin-Aldosterone System (RAAS): Renal hypoperfusion triggers renin release from juxtaglomerular cells. Angiotensin II induces potent vasoconstriction and stimulates aldosterone secretion from the adrenal cortex, driving renal sodium and water retention, myocardial fibrosis, and ventricular stiffening.
3. Natriuretic Peptide Counter-regulation: Ventricular wall stretch stimulates secretion of B-type natriuretic peptide (BNP) and its biologically inactive cleaved byproduct, NT-proBNP. These peptides promote natriuresis, diuresis, and vasodilation, but their effects are ultimately overwhelmed by hyperactive RAAS and sympathetic tone.

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2. Acute Decompensated Heart Failure (ADHF)

Clinical Presentation

Patients typically present with severe respiratory distress and volume overload:

• Left-Sided Congestion (Pulmonary Venous Hypertension): Severe exertional dyspnoea, orthopnoea (breathlessness when lying flat, measured by the number of pillows required), paroxysmal nocturnal dyspnoea (PND; waking gasping for air 1–2 hours after sleep), tachypnoea, cough producing pink frothy sputum in frank pulmonary oedema, and extensive bilateral inspiratory crackles on auscultation (starting at the lung bases and extending upwards).
• Right-Sided Congestion (Systemic Venous Overload): Elevated jugular venous pressure (JVP), positive hepatojugular reflux, tender hepatomegaly, bilateral pitting peripheral oedema (pedal, pretibial, or sacral if recumbent), and ascites.
• Cardiac Auscultation: S3 gallop rhythm (a low-frequency third heart sound in early diastole caused by rapid passive filling into a stiff, dilated, volume-overloaded ventricle; highly specific for elevated filling pressures), displaced and diffuse apex beat, and functional mitral or tricuspid regurgitation murmurs.

Diagnostic Evaluation

• Serum NT-proBNP: The investigation of choice to rule out heart failure. In acute presentations with acute dyspnoea, NT-proBNP <300 pg/mL has an extraordinary negative predictive value (>98%), safely ruling out heart failure. In non-acute (chronic) settings, NICE NG106 states that an NT-proBNP below 400 ng/L (equivalent to pg/mL) in an untreated person makes heart failure less likely (the ESC uses below 125 pg/mL to rule out). An NT-proBNP above 2,000 ng/L needs urgent specialist assessment and transthoracic echocardiography within 2 weeks; 400–2,000 ng/L needs them within 6 weeks.
  • Confounding Factors: Natriuretic peptides are elevated by advanced age, female sex, renal impairment, atrial fibrillation, and systemic sepsis. Levels are paradoxically reduced by obesity.
• Chest Radiography (The ABCDE Mnemonic):
  • A — Alveolar Oedema: Perihilar "bat's wing" or "butterfly" dense bilateral opacities.
  • B — Kerley B Lines: Short (1–2 cm), thin, horizontal peripheral interstitial lines perpendicular to the pleural surface at the costophrenic angles, reflecting distended interlobular lymphatics.
  • C — Cardiomegaly: Cardiothoracic ratio (CTR) >0.5 on a standard posteroanterior (PA) erect film.
  • D — Dilated Upper Lobe Vessels: Upper lobe blood diversion (cephalisation), where pulmonary veins in the upper zones equal or exceed lower zone vessel calibre.
  • E — Pleural Effusions: Blunting of costophrenic angles, typically bilateral or right-sided predominance.
• Transthoracic Echocardiography (TTE): Mandatory in all cases to quantify LVEF, measure chamber dimensions, calculate wall thickness, evaluate valvular integrity, and assess pulmonary artery systolic pressure.

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3. Acute Management of Pulmonary Oedema

Acute heart failure is an immediate medical emergency. Management follows a structured decongestion protocol:

1. Positioning: Sit the patient upright in bed with legs dangling over the edge if tolerated, immediately reducing systemic venous return (preload).
2. Controlled Oxygenation: High-flow oxygen should not be given routinely. Administer supplemental oxygen only if SpO2 <94% (or target 88–92% if at risk of hypercapnic respiratory failure). Unnecessary hyperoxia induces systemic vasoconstriction and worsens coronary perfusion.
3. Intravenous Loop Diuretics:
   • Furosemide 40–80 mg IV bolus (or Bumetanide 1–2 mg IV). If the patient is already taking maintenance oral loop diuretics, the initial IV bolus dose should equal 1 to 2.5 times their total daily oral dose.
   • Assess clinical response and spot urinary sodium at 2 hours and total urine output at 6 hours (target >100–150 mL/hour). If diuresis is inadequate, double the IV furosemide dose or add a thiazide-like diuretic (e.g. oral metolazone or IV chlorothiazide) to achieve synergistic sequential nephron blockade.
4. Vasodilators (Intravenous Nitrates):
   • Intravenous glyceryl trinitrate (GTN) or isosorbide dinitrate infusion is not offered routinely in acute heart failure (NICE CG187). It is used in specific circumstances: concomitant myocardial ischaemia, severe hypertension, or regurgitant aortic or mitral valve disease, with close blood pressure monitoring (ESC guidance considers vasodilators when systolic BP is above 110 mmHg).
   • Titrate starting at 10–20 mcg/min, monitoring blood pressure every 5 minutes. Avoid completely if systolic BP is <90–100 mmHg.
5. Non-Invasive Ventilation (NIV / CPAP):
   • Continuous positive airway pressure (CPAP at 5–10 cmH2O) or bilevel positive airway pressure (BiPAP) should be considered promptly if the patient exhibits persistent severe dyspnoea, tachypnoea, hypoxaemia, and respiratory acidosis despite pharmacotherapy. CPAP increases intrathoracic pressure, reduces venous return, decreases LV afterload, and recruits fluid-filled alveoli.
6. Avoid Routine Opiates: Routine use of intravenous opiates (morphine/diamorphine) is no longer recommended by ESC or NICE guidelines due to proven associations with respiratory depression, increased rates of invasive mechanical ventilation, and worse clinical outcomes. Reserve strictly for selected patients with intractable distress or terminal palliation.

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4. Chronic HFrEF: The "Fantastic Four" Guideline-Directed Therapy

In chronic HFrEF (LVEF ≤40%), modern guidelines mandate early, rapid introduction of four foundational drug classes—often termed the "Fantastic Four"—each demonstrating independent, additive reductions in all-cause mortality, cardiovascular death, and heart failure hospitalisation.

Adjunctive & Device Therapies

• Loop Diuretics: Furosemide or bumetanide titrated to the lowest effective dose to maintain euvolaemia. Note: Loop diuretics alleviate congestive symptoms but do not confer a mortality benefit.
• Ivabradine: Selective sinus node If ("funny" current) inhibitor. Indicated in patients in normal sinus rhythm with resting heart rate ≥70 bpm and LVEF ≤35% despite receiving maximum tolerated target doses of beta-blockers.
• Implantable Cardioverter-Defibrillator (ICD): Indicated for primary prevention of sudden cardiac death in patients with symptomatic HFrEF (NYHA class II–III) and LVEF ≤35% despite at least 3 months of optimal guideline-directed medical therapy, provided life expectancy exceeds 1 year.
• Cardiac Resynchronisation Therapy (CRT): Biventricular pacing indicated for patients with LVEF ≤35%, NYHA II–IV symptoms despite optimal GDMT, and complete Left Bundle Branch Block (LBBB) with QRS duration ≥130–150 ms in sinus rhythm, to reverse electromechanical dyssynchrony.

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5. Cardiogenic Shock

Cardiogenic shock represents the extreme end of the heart failure spectrum, characterised by profound primary cardiac pump failure resulting in critical systemic tissue hypoperfusion.

Diagnostic Criteria

• Sustained Hypotension: Systolic BP <90 mmHg for >30 minutes (or mean arterial pressure [MAP] <65 mmHg), or requirement for vasopressors to maintain SBP ≥90 mmHg.
• Evidence of End-Organ Hypoperfusion:
  • Oliguria (urine output <0.5 mL/kg/hour).
  • Cold, clammy, cyanotic peripheries and delayed capillary refill (>3 seconds).
  • Altered mental status (lethargy, agitation, encephalopathy).
  • Hyperlactataemia (serum arterial lactate >2.0 mmol/L) reflecting widespread anaerobic metabolism.
• Haemodynamic Profile: Severely reduced cardiac index (<2.2 L/min/m2) in the presence of elevated pulmonary capillary wedge pressure (PCWP >15 mmHg), confirming pump failure rather than hypovolaemic shock.

Management Strategy

1. Early Revascularisation: The SHOCK trial confirmed that emergent PCI or CABG significantly improves survival when acute myocardial infarction is the underlying cause (~80% of cardiogenic shock cases).
2. Inotropic Support: Intravenous Dobutamine (beta-1 agonist with mild beta-2 and alpha-1 activity) is first-line to enhance myocardial contractility and stroke volume. Alternative: Milrinone (phosphodiesterase-3 inhibitor, useful if on chronic beta-blockers, but causes peripheral vasodilation).
3. Vasopressor Support: Noradrenaline (norepinephrine) is the vasopressor of choice when marked hypotension threatens coronary perfusion, titrated to maintain MAP ≥65 mmHg.
4. Mechanical Circulatory Support (MCS): Early escalation to temporary mechanical assist devices: Intra-Aortic Balloon Pump (IABP), percutaneous microaxial ventricular assist devices (Impella), or Veno-Arterial Extracorporeal Membrane Oxygenation (VA-ECMO) as a bridge to recovery, revascularisation, or heart transplantation.