Heart failure assessment and treatment

Heart Failure, Cardiogenic Shock & Cardiac Arrhythmias

Heart failure (HF) and cardiac arrhythmias represent major causes of emergency hospital admissions and cardiovascular morbidity across Australia. Effective management requires precise phenotypic classification, rapid initiation of mortality-reducing guideline-directed medical therapy (GDMT), and timely stabilization of haemodynamic decompensation and electrical instability.

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Heart Failure Phenotypes and Diagnostic Evaluation

Heart failure is a complex clinical syndrome characterized by cardinal symptoms (breathlessness, orthopnoea, fatigue, ankle swelling) and clinical signs (elevated jugular venous pressure, pulmonary crackles, peripheral oedema) caused by a structural or functional cardiac abnormality that results in elevated intracardiac pressures or reduced cardiac output.

According to the universal definition and Australian guidelines, heart failure is classified into three distinct phenotypes based on left ventricular ejection fraction (LVEF):

1. Heart Failure with Reduced Ejection Fraction (HFrEF): $LVEF \le 40\%$. Characterized by impaired myocardial contractility, progressive ventricular dilatation, and eccentric remodelling. Quadruple medical therapy substantially reduces mortality and hospital admissions.
2. Heart Failure with Mildly Reduced Ejection Fraction (HFmrEF): $LVEF \text{ } 41\%\text{ to }49\%$. Represents a transitional phenotype that shares clinical characteristics and therapeutic responsiveness with HFrEF.
3. Heart Failure with Preserved Ejection Fraction (HFpEF): $LVEF \ge 50\%$ with objective evidence of diastolic dysfunction, structural alterations (left atrial enlargement, left ventricular hypertrophy), or elevated resting/exertional left ventricular filling pressures.

Diagnostic Biomarkers & Imaging

• B-type Natriuretic Peptide (BNP) & N-Terminal pro-BNP (NT-proBNP): Released by ventricular myocytes in response to increased wall stress and volume expansion. Highly sensitive rule-out biomarkers in the acute presentation:
  • Acute setting: $BNP < 100\text{ pg/mL}$ or $NT\text{-}proBNP < 300\text{ pg/mL}$ reliably excludes acute heart failure (negative predictive value $> 95\%$).
  • Confounders: Levels are elevated by advanced age, renal impairment ($eGFR < 60\text{ mL/min/1.73m}^2$), and atrial fibrillation. Conversely, levels are disproportionately lower in obese patients ($BMI \ge 30\text{ kg/m}^2$).
  • Clinical Caveat: Sacubitril inhibits neprilysin (the enzyme that degrades BNP). Consequently, patients receiving sacubitril/valsartan have elevated circulating BNP levels; NT-proBNP must be measured instead to assess clinical response, as NT-proBNP is not a neprilysin substrate.
• Transthoracic Echocardiography (TTE): The gold standard non-invasive diagnostic investigation. Evaluates LVEF, chamber dimensions, regional wall motion abnormalities, valvular lesions, and markers of diastolic filling pressures (mitral inflow $E/A$ ratio, tissue Doppler $E/e'$ ratio, and tricuspid regurgitant jet velocity for estimating pulmonary artery systolic pressure).
• Chest Radiography: Identifies signs of pulmonary venous congestion and fluid overload:
  • Cardiomegaly: Cardiothoracic ratio $> 0.50$ on a posterior-anterior view.
  • Vascular redistribution: Upper lobe venous diversion ("stag's antler sign").
  • Interstitial oedema: Peribronchial cuffing and horizontal linear densities at the lung bases (Kerley B lines).
  • Alveolar oedema: Bilateral perihilar opacities in a classic "bat-wing" or "butterfly" distribution.
  • Pleural effusions: Usually bilateral or right-sided greater than left-sided.

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Guideline-Directed Medical Therapy (GDMT) for HFrEF

Australian guidelines (NHFA/CSANZ) endorse early, concurrent initiation and up-titration of the "Fantastic Four" foundational pillars of quadruple therapy for all patients with HFrEF ($LVEF \le 40\%$) to reduce mortality and hospitalizations:

1. Angiotensin Receptor-Neprilysin Inhibitor (ARNI) or ACE Inhibitor:
   • Sacubitril/valsartan is preferred first-line over ACE inhibitors based on the landmark PARADIGM-HF trial, which demonstrated a 20% relative reduction in cardiovascular death and heart failure hospitalization.
   • Critical Safety Rule: When switching a patient from an ACE inhibitor to sacubitril/valsartan, a mandatory 36-hour washout period is required between the last dose of the ACE inhibitor and the first dose of sacubitril/valsartan. Concomitant inhibition of ACE and neprilysin results in excessive bradykinin accumulation, causing catastrophic, life-threatening angioedema. A washout period is not required when switching from an Angiotensin Receptor Blocker (ARB).
   • If ARNI is not tolerated or subsidized, an ACE inhibitor (e.g., ramipril, perindopril) or ARB (e.g., candesartan) should be titrated to target doses.
2. Evidence-Based Beta-Blockers:

• HFrEF beta-blockade: Use an agent supported by heart failure evidence and titrate in a stable patient. Choice depends on comorbidity, blood pressure and local guidance; avoid presenting a short list as the only agents with any evidence.
  • Must be initiated at low doses only when the patient is clinically stable and euvolaemic, with slow dose doubling every 2 to 4 weeks under close observation for transient fluid retention.

1. Mineralocorticoid Receptor Antagonists (MRAs):
   • Spironolactone ($25\text{ to }50\text{ mg}$ daily) or eplerenone ($25\text{ to }50\text{ mg}$ daily).
   • Serum potassium and creatinine must be checked at baseline, 1 week, 4 weeks, and then every 3 months. Therapy must be withheld or dose halved if serum potassium exceeds $5.5\text{ mmol/L}$ or if renal function declines acutely.
2. Sodium-Glucose Cotransporter-2 (SGLT2) Inhibitors:
   • Dapagliflozin ($10\text{ mg}$ once daily) or empagliflozin ($10\text{ mg}$ once daily).
   • SGLT2 inhibitors reduce heart-failure events across reduced, mildly reduced and preserved ejection fractions. Do not describe the composite benefit as proof of mortality reduction alone in every phenotype; also manage congestion and comorbid disease.

Device Therapies in HFrEF

• Implantable Cardioverter-Defibrillator (ICD): Indicated for primary prevention of sudden cardiac death in patients with symptomatic HFrEF ($LVEF \le 35\%$, NYHA Class II–III) despite at least 3 months of optimal GDMT, provided expected meaningful survival exceeds 1 year.
• Cardiac Resynchronization Therapy (CRT-P / CRT-D): Indicated for patients with $LVEF \le 35\%$, sinus rhythm, and complete Left Bundle Branch Block (LBBB) with a QRS duration $\ge 130\text{ to }150\text{ ms}$ despite optimal medical therapy, to restore ventricular mechanical synchrony.

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Acute Decompensated Heart Failure & Cardiogenic Shock

Acute decompensated heart failure (ADHF) is classified using the Stevenson 2x2 hemodynamic matrix based on clinical bedside evaluation of perfusion ("warm" vs "cold") and congestion ("dry" vs "wet"):

• Warm & Wet (Most Common, ~80%): Adequate peripheral perfusion with pulmonary and systemic congestion (elevated JVP, crepitations, peripheral oedema). Managed with intravenous loop diuretics and vasodilators.
• Cold & Wet (Cardiogenic Shock, ~10%): Poor peripheral perfusion (hypotension, oliguria, cold mottled extremities, altered mental status, lactic acidosis) with systemic congestion. Requires inotropic support, vasopressors, and mechanical circulatory support.
• Cold & Dry (~5%): Hypoperfusion without congestion. Typically results from excessive diuresis; requires cautious fluid resuscitation.
• Warm & Dry (~5%): Compensated, euvolaemic state on optimal therapy.

Emergency Management of Acute Pulmonary Oedema

1. Positioning & Oxygenation: Sit the patient fully upright. Administer supplemental oxygen only if $SpO_2 < 93\%$.

• Non-invasive ventilation: In appropriate acute cardiogenic pulmonary oedema, positive airway pressure recruits alveoli, reduces respiratory work and can reduce cardiac loading. It requires close monitoring; shock, inability to protect the airway or failure to improve may require another approach.

1. Intravenous Loop Diuretics: Administer intravenous furosemide ($40\text{ to }80\text{ mg}$ IV bolus, or $1\text{ to }2\text{ times}$ the patient's daily home oral dose). Diuretics produce rapid venodilation within minutes, followed by diuresis at 20 to 30 minutes.
2. Intravenous Vasodilators: If systolic blood pressure is $> 110\text{ mmHg}$, administer sublingual or intravenous glyceryl trinitrate (starting at $10\text{ to }20\text{ mcg/min}$ and titrating upward every 3 to 5 minutes). Nitrates rapidly reduce systemic venous return (preload) and left ventricular filling pressures.
3. Opioid Policy: Routine administration of intravenous morphine is no longer recommended in Australian acute heart failure guidelines, as registry data demonstrate an association with increased intubation rates, ICU admissions, and in-hospital mortality.

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Primary references (checked 7 October 2026): Heart Foundation AF resources.