Inpatient Management of Chronic Heart Failure With Preserved Ejection Fraction

Chronic heart failure with preserved ejection fraction (HFpEF) is a common reason for hospital admission, yet it can be harder to recognise than heart failure with reduced ejection fraction. Patients may arrive with breathlessness, oedema, fatigue or exercise intolerance while the left ventricular ejection fraction remains normal. The clinical problem is impaired filling, raised filling pressures and limited cardiovascular reserve rather than a weak ventricular contraction alone.

The HM17 review of inpatient management is especially useful because it places acute treatment within the wider realities of hospital medicine: medication reconciliation, renal function, fluid balance, comorbidity management, communication between teams and safe discharge. A normal ejection fraction should never be used to dismiss congestion or to delay treatment while the team searches for a single explanatory diagnosis.

For Australian clinicians, the same principles apply across a metropolitan ward in Melbourne, a tertiary service in Sydney and a smaller regional hospital managing transfers. Local factors shape the details. Medicare-funded follow-up, Pharmaceutical Benefits Scheme access, electronic medication systems and the distance between rural patients and specialist clinics all influence whether a sound inpatient plan remains workable after discharge.

The following review focuses on bedside decisions rather than a single drug protocol. It considers how to confirm the syndrome, relieve congestion, manage common triggers and prepare patients for ongoing care. It also reflects the educational setting of the 2017 Society of Hospital Medicine meeting, when evidence for HFpEF-specific therapies was still developing.

Defining The Inpatient Problem

HFpEF usually involves a left ventricular ejection fraction of at least 50%, symptoms or signs of heart failure, and evidence of elevated filling pressures or structural heart disease. Older age, hypertension, atrial fibrillation, obesity, diabetes, chronic kidney disease and coronary disease frequently cluster in the same patient. This combination creates a vulnerable circulation that may decompensate after a relatively small insult.

The admission diagnosis should therefore describe both the syndrome and its likely trigger. Acute pulmonary oedema after uncontrolled hypertension is a different clinical situation from gradual peripheral oedema caused by missed diuretics, although both may occur with preserved ejection fraction. Infection, myocardial ischaemia, rapid atrial fibrillation, anaemia, pulmonary embolism, renal deterioration and excess dietary sodium deserve active consideration.

Symptoms can be disproportionate to examination findings. Obesity may obscure jugular venous distension, while chronic lung disease can make crackles difficult to interpret. A previously documented echocardiogram is helpful, but the current presentation still requires a fresh assessment of volume status and precipitating factors.

Recognising Congestion And Its Triggers

Breathlessness when lying flat, nocturnal dyspnoea, rapid weight gain, elevated jugular venous pressure, hepatomegaly and dependent oedema support congestion. Lung ultrasound, chest radiography, natriuretic peptides and point-of-care echocardiography can strengthen the assessment, although each has limitations. Natriuretic peptide concentrations may be lower in obesity and higher with renal impairment or atrial fibrillation.

Blood pressure is a central clue. Some patients with HFpEF present with severe hypertension and flash pulmonary oedema, while others are hypotensive after over-diuresis or a medication error. A careful comparison with the patient’s usual weight, blood pressure, creatinine and diuretic dose is often more informative than an isolated abnormal result.

The medical history should include fluid intake, alcohol, over-the-counter medicines and recent changes in mobility. Ibuprofen and other non-steroidal anti-inflammatory drugs can worsen renal sodium retention. In Australia, frequent takeaway meals, packaged foods and large portions can produce a high sodium load even when a patient reports avoiding the salt shaker.

Assessing The First 24 Hours

Initial management combines oxygen or ventilatory support when indicated with prompt treatment of congestion and the precipitating illness. Intravenous loop diuretics are commonly required when oral absorption is unreliable or the patient is clearly overloaded. The starting dose should reflect the home dose, renal function, prior response and severity of presentation, followed by reassessment rather than passive continuation.

Urine output, symptoms, respiratory effort, blood pressure, renal function, electrolytes and daily weight provide a practical monitoring set. A modest creatinine rise during effective decongestion does not automatically mean that treatment has failed. Conversely, worsening renal function with persistent congestion may signal inadequate diuretic delivery, venous congestion or an unrecognised trigger.

Fluid and sodium advice should be individualised. Severe blanket restriction can cause thirst, poor intake and distress without improving outcomes for every patient. A fluid limit may be reasonable for marked congestion or hyponatraemia, but it should be documented with a clear review point.

Managing Comorbidities And Medicines

HFpEF care is largely care of the whole cardiovascular patient. Blood pressure control reduces afterload and may prevent recurrent decompensation. Atrial fibrillation requires attention to rate, rhythm, stroke prevention and the effect of loss of atrial contraction on filling. Ischaemia, valvular disease, sleep-disordered breathing and pulmonary hypertension should be evaluated when clinically relevant.

Diabetes, obesity and chronic kidney disease complicate both diagnosis and treatment. Medication doses need review as renal function changes, and the team should distinguish an appropriate temporary hold from an indefinite cessation. Mineralocorticoid receptor antagonists and renin-angiotensin system medicines may be useful in selected patients, but potassium and renal monitoring are essential.

The HM17 educational context also reinforces the importance of electrolyte safety. A focused hyperkalaemia management review is relevant when kidney disease, potassium supplements or interacting medicines accompany decompensated heart failure. Australian hospitals should also check the inpatient medication chart against the patient’s actual medicines, recent community dispensing and the PBS supply pathway.

Beta blockers should not be reflexively stopped or escalated. The decision depends on perfusion, congestion, heart rate and the reason for treatment. Digoxin, antiarrhythmics, insulin, opioids and sedatives each carry additional risks in older people with impaired renal clearance. Medication reconciliation should include non-prescription products and medicines obtained from multiple pharmacies.

Building A Safe Discharge Plan

Discharge should follow clinical stability rather than an arbitrary number of inpatient days. The patient should have a clear oral diuretic regimen, stable or improving symptoms, a plan for renal and electrolyte testing, and an explanation of which medicines were changed and why. Weight monitoring is useful when the patient can perform it consistently and knows whom to contact if weight rises.

A discharge summary needs to communicate the admission trigger, dry-weight estimate, treatment response, echocardiography findings, renal trend and pending investigations. It should identify the clinician responsible for follow-up. In Australia, coordination may involve a hospital cardiology service, the general practitioner, a community pharmacist, a heart failure nurse and Aboriginal or Torres Strait Islander health services, depending on the patient’s circumstances.

Access is a clinical issue. Someone living in inner Sydney may obtain pathology and specialist review quickly, while a patient in regional Queensland may face a long drive, limited public transport or delayed appointments. A plan that depends on frequent laboratory testing must account for those realities. Telehealth, local pathology collection and communication with the GP can make monitoring more practical.

The discharge conversation should cover sodium-rich foods, alcohol, activity, vaccinations, NSAID avoidance and early warning symptoms. Advice is more effective when connected to everyday habits, such as reading labels on supermarket meals or recognising that restaurant and takeaway food can contain substantial sodium.

Translating HM17 Learning Into Practice

The HM17 conference archive provides useful historical context for the meeting’s emphasis on practical education, research, patient care and professional collaboration. For HFpEF, the enduring lesson is that high-quality inpatient care depends on repeated clinical reassessment rather than a single echocardiographic number or a rigid algorithm.

A hospitalist-led approach can bring together nursing observations, pharmacy review, allied health input and specialist advice. Nurses may identify worsening orthopnoea or poor urine output before the next medical review. Pharmacists can detect duplicate antihypertensives, potassium-containing products or a mismatch between the prescribed and supplied diuretic. Physiotherapists and occupational therapists can help distinguish cardiopulmonary limitation from deconditioning.

Care should also be culturally safe and practical. Treatment explanations need to accommodate health literacy, language, family involvement and patient preferences. For Aboriginal and Torres Strait Islander patients, partnership with culturally appropriate services may improve trust and continuity. These considerations are part of safe heart failure management, not additional administrative work.

Bedside Priorities For Australian Wards

A concise ward checklist can reduce missed details during a busy admission:

• Confirm congestion, ejection fraction history and the likely precipitating illness.
• Record baseline weight, renal function, potassium, blood pressure and home diuretic exposure.
• Reassess response to intravenous diuresis using symptoms, urine output, examination and laboratory trends.
• Review NSAIDs, supplements, potassium-raising medicines and drugs affected by renal impairment.
• Arrange realistic pathology, GP or specialist follow-up before discharge, including a named responsible clinician.

The checklist should support judgement rather than replace it. A patient who remains visibly congested needs a treatment response, even if the creatinine has changed modestly. A patient who is euvolaemic but dizzy, hypotensive or increasingly azotaemic needs a different response from someone with persistent pulmonary oedema.

HFpEF remains a syndrome requiring careful phenotyping, trigger treatment and prevention of recurrent admissions. The practical next step is to add a documented congestion assessment, medication reconciliation and post-discharge blood-test plan to the ward round for the next admitted patient with preserved ejection fraction.