Building a Heart Failure Clinic: The Model That Standardises Care

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.

A full package before the four pillars of therapy are started together: pro-BNP, full blood count, renal and liver function, thyroid function, a 12-lead ECG and a chest X-ray.

A 12-lead ECG, which tracks the electrical progression of myocardial disease through QRS broadening and eventual bundle branch block, and a pro-BNP, which can flag silent fluid overload before symptoms return.

They are assessed for cardiac resynchronisation therapy and an implantable defibrillator. If they exhaust those options too, the pathway moves to advanced cardiac MRI, biopsy where indicated, and formal transplant or ventricular assist device assessment.

The nurse is assigned to each patient with clear instructions on when to recheck renal function and when to bring the patient back in urgently, functioning as the ongoing point of contact between visits.

Once a patient has exhausted every medical and device option and continues to decline, a comfort-focused conversation is considered appropriate rather than further escalation.