The Four Stages of Heart Failure: Catching Patients Before Symptoms Start

The mechanism is glycosuria, which is a nidus for genitourinary infections — balanitis in men and UTIs in women, at an incidence of around 5 to 6%. Counsel every patient on personal and perineal hygiene when starting the drug. If a genitourinary infection develops, get a urine culture, and if confirmed, hold the SGLT2 inhibitor until it resolves, then restart with reinforced hygiene counselling.

There is no substantial long-term beneficial role — it is like flogging a dead horse, a transient cardiac output boost without sustained benefit. It's useful only as a short-term emergency bridge for a profoundly hypotensive patient. We now more routinely use noradrenaline rather than dobutamine in acute low-output heart failure.

The Sgarbossa criteria identify acute myocardial infarction in the presence of a left bundle branch block, where it is otherwise difficult to tell whether ECG changes represent an acute MI or simply the LBBB pattern — specifically, 4mm or more of ST elevation discordant to the QRS is considered an acute MI regardless of the LBBB. This is used specifically in the context of chest pain with LBBB, not in the context of established heart failure management.

A failing heart relies on two compensatory mechanisms: increased heart rate and elevated blood pressure. A beta blocker reduces both, so cardiac output falls initially and the patient feels rough — but only for the first one to two weeks. After that, sustained reduction in neurohormonal activation reverses adverse cardiac remodelling and the patient improves steadily. Always counsel patients about this dip in advance and reassure them it will get better; a heart failure nurse is an excellent resource for this kind of communication.

BNP and NT-proBNP are released in response to myocardial wall stress, so a normal BNP with a normal ECG makes acute heart failure very unlikely as the cause of a patient's breathlessness — the dyspnoea is most likely pulmonary or another non-cardiac cause. One nuance: in a patient presenting late, days after the onset of acute heart failure while partially compensating, BNP can occasionally read lower than expected, so very recent-onset context still matters.

Patients with obesity, hypertension, diabetes, a smoking or alcohol history, a family history of premature vascular disease or cardiomyopathy, a prior MI or unstable angina, or exposure to cardiotoxic chemotherapy. An ECG, echocardiogram and pro-BNP once a year is the recommended prophylactic approach.

Structural heart disease with minimal or no symptoms, such as rheumatic mitral disease with elevated filling pressures. A natriuretic peptide of 800 to 1,200, even without symptoms, signals developing heart failure that is worth treating early.

Because its onset in this group is genuinely insidious. Patients often don't realise anything is wrong until the disease has already progressed.

Patients who have missed the earlier stages entirely and present with orthopnoea, paroxysmal nocturnal dyspnoea and repeat hospital admissions, by which point treatment options have narrowed considerably.