Practice Points on Heart Failure

Posted: July 24, 2024

Author: Dr Selwyn Wong

Heart failure (HF) is a common (1-3%) clinical issue that continues to cause significant hospitalisation and mortality in NZ.  Presentation is varied and the diagnosis is based on multiple clinical features. History is important.

Symptoms are caused by decreased cardiac output (fatigue, dyspnoea) or congestion from increased cardiac filling pressures (orthopneoa, paroxysmal nocturnal dyspnoea and oedema).

Clinical examination findings from decreased output include hypotension, cool peripheries and those from congestion, lung crackles and peripheral oedema.

Basic general practice tests should include haemoglobin, electrolytes, renal and liver function, thyroid function and brain naturetic pepetide (BNP). Additionally, where possible, an ECG and CXR.

Causation

HF describes the clinical syndrome but not the underlying cause. A pivotal categorisation requires an echocardiographic quantification of left ventricular function using ejection fraction (EF) (reduced EF ≤ 40%, mid-range EF 41-49% and preserved EF ≥50%).

The cause of reduced ejection fraction is most commonly coronary artery disease i.e. ischaemic cardiomyopathy. The remainder are non-ischaemic cardiomyopathy with common causes including hypertension, alcohol/methamphetamine, valvular heart disease, tachyarrythmia (including atrial fibrillation/flutter), virus (e.g. COVID), drugs (e.g.chemotherapy, clozapine). Common causes of HFpEF include hypertension, age, obesity and diabetes. Reversal of any underlying cause is important e.g. CABG for those with an ischaemic cardiomyopathy.

Pharmacotherapy

Diuretics can reduce symptoms of congestion. Fluid intake should not be excessive.
In HFrEF four drug classes should be instituted and uptitrated to maximum tolerated dose.
These are renin-angiotensin system antagonist (ACE inhibitor or ARB] or the ARB and neprilysin inhibitor combination [ARNI], beta-blockers (bisoprolol, metoprolol or carvedilol), mineralocorticoid receptor antagonist (MRA) (spironolactone or eprelenone) and the sodium-glucose-cotransporter-2 (SGLT2) inhibitor (empagliflozin)

Limitations to uptitration are symptomatic hypotension, hyperkalaemia and significantly worsening renal function. However, each class of drug can improve LV function and prolong life expectancy – hence aggressive and persistent optimisation of medication is vital.

In HFmrEF or HFpEF, only SGLT2 inhibitors have been shown to improve outcomes.
At current time, SGLT2 inhibitors are funded only in diabetic patients but patients should be asked about self-funding this medicine.

Conclusion

  • Heart failure is a combination of clinical features.
  • Quantification of ejection fraction is vital.
  • Optimal pharmacotherapy has important outcome benefits including mortality.
  • Suboptimal HF workforce numbers in NZ necessitates general practice to have key role in HF management particularly in optimisation of pharmacotherapy.

References and Further Reading

(1) 2023 position statement on improving management for patients with heart failure in Aotearoa New Zealand 2024 Feb 23; 137(1590). ISSN 1175-8716 https://www.nzmj.org.nz/

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