8.1 Hypertension & Heart Failure
Key Takeaways
- First-line antihypertensives for many adults are ACE inhibitors or ARBs, dihydropyridine calcium channel blockers, and thiazide-like diuretics, often used in combination when monotherapy is insufficient.
- ACE inhibitors and ARBs require monitoring of serum potassium and creatinine after initiation or dose increase; dry cough and angioedema are key ACE-inhibitor adverse effects.
- HFrEF guideline-directed pillars at exam level include ACEI/ARB/ARNI concepts, evidence-based beta-blockers, mineralocorticoid receptor antagonists, and SGLT2 inhibitors, plus loop diuretics for congestion.
- Fluid-overload counselling focuses on daily weight, salt and fluid guidance, and early recognition of rising oedema or dyspnoea.
- Red flags such as acute pulmonary oedema, chest pain suggestive of ACS, severe symptomatic hypotension, and angioedema require urgent referral rather than routine community optimisation alone.
8.1 Hypertension & Heart Failure
Quick Answer: For hypertension, know first-line Australian options—ACE inhibitors (ACEI) or angiotensin receptor blockers (ARBs), dihydropyridine calcium channel blockers (CCBs), and thiazide-like diuretics—and when to combine rather than escalate a single agent endlessly. Monitor potassium and creatinine with renin–angiotensin system blockers. For heart failure with reduced ejection fraction (HFrEF), think in pillars: ACEI/ARB/ARNI concepts, evidence-based beta-blockers, mineralocorticoid receptor antagonists (MRAs), and SGLT2 inhibitors, with loop diuretics for fluid overload. Counsel on weight, salt/fluid, adherence, and red flags that need urgent care.
Cardiovascular therapeutics sit at the centre of National Competency Standards 3.2 (implement medication management) and 3.3 (monitor and evaluate). Intern Written items rarely ask you to invent a full regimen from scratch; they test whether you can choose a safe class, spot monitoring gaps, counsel for adherence and adverse effects, and refer when the presentation is unstable.
Hypertension — first-line medicines
Australian practice (AMH and local guidelines) commonly positions three classes as first-line options for uncomplicated essential hypertension in many adults:
| Class | Examples (AU names) | Typical role | Key counselling / monitoring |
|---|---|---|---|
| ACE inhibitors | perindopril, ramipril, enalapril, lisinopril | First-line; preferred if diabetes with albuminuria, HFrEF, post-MI context | Dry cough, hyperkalaemia, rise in creatinine, rare angioedema; avoid in pregnancy |
| ARBs | candesartan, irbesartan, telmisartan, valsartan | Alternative when ACEI not tolerated (especially cough) | Hyperkalaemia, creatinine rise; pregnancy contraindication; much lower cough risk than ACEI |
| Dihydropyridine CCBs | amlodipine, lercanidipine, felodipine | First-line alternative or add-on | Ankle oedema, flushing, headache; no routine K+/Cr class effect like ACEI/ARB |
| Thiazide-like diuretics | indapamide; hydrochlorothiazide still seen | First-line alternative or combination backbone | Electrolytes, uric acid/gout risk, volume depletion in elderly |
Exam framing: Do not treat “first-line” as one universal tablet for every patient. Choice is modified by comorbidities (diabetes with nephropathy, heart failure, ischaemic heart disease, gout, asthma/COPD for some beta-blockers), age and frailty, ethnicity considerations discussed in guidelines, pregnancy potential, and concurrent medicines.
Combination therapy
Many patients need two agents from complementary classes rather than maximal titration of a poorly effective monotherapy. Rational combinations often pair:
- ACEI or ARB + CCB
- ACEI or ARB + thiazide-like diuretic
- CCB + thiazide-like diuretic
Avoid dual ACEI + ARB as routine combination therapy—increased renal and hyperkalaemia risk without clear outcome benefit in general hypertension. Fixed-dose combinations can improve adherence when strengths match clinical need. When blood pressure remains high despite two agents, review adherence, white-coat effect, secondary causes, and then add a third agent rather than assuming “max dose of one drug” is always best.
Monitoring potassium and creatinine (ACEI/ARB)
Renin–angiotensin system blockade can reduce glomerular filtration pressure and raise potassium. Intern-level monitoring principles:
- Check baseline electrolytes and renal function when starting or substantially increasing dose.
- Recheck after initiation/up-titration (commonly within days to a few weeks—use AMH/local protocol timing).
- Expect a modest creatinine rise in some patients; large rises, progressive decline, or significant hyperkalaemia need dose reduction, temporary hold, review of interacting drugs (e.g. potassium supplements, potassium-sparing diuretics, NSAIDs), and medical review.
- Counsel patients not to use NSAIDs casually for pain without advice—the “triple whammy” of ACEI/ARB + diuretic + NSAID is a classic acute kidney injury pattern.
ACE inhibitor cough and angioedema
- Dry cough is a common reason to switch ACEI → ARB if cough is clearly drug-related and alternative causes (heart failure, infection, ACEI timing coincidence) are considered.
- Angioedema (facial, lip, tongue, airway swelling) is uncommon but potentially life-threatening. Treat as a medical emergency if airway involvement; permanently avoid ACE inhibitors after true angioedema. ARB cross-risk is low but not zero—specialist input is needed for complex history.
Heart failure with reduced ejection fraction (HFrEF)
At exam depth, HFrEF management is organised as foundational pillars that reduce hospitalisation and mortality when indicated, plus symptom-directed diuretics for congestion.
Pillar concepts (exam level)
| Pillar | Concept | Intern counselling / monitoring notes |
|---|---|---|
| ACEI / ARB / ARNI | ACEI traditionally first; ARB if ACEI intolerant; ARNI (sacubitril/valsartan) is a specialised renin–angiotensin pathway option used per specialist/guideline criteria and washout rules from ACEI | Hypotension, K+, renal function; never combine ARNI with ACEI |
| Evidence-based beta-blockers | In HFrEF, focus on agents with outcome evidence (e.g. bisoprolol, carvedilol, nebivolol, metoprolol succinate where used) rather than any beta-blocker for rate control alone | Start low, go slow; warn about temporary fatigue/dizziness; do not stop abruptly; caution in decompensated fluid overload |
| MRA | Spironolactone or eplerenone for eligible HFrEF patients | Hyperkalaemia, renal function, gynaecomastia (spironolactone); counsel on K+ awareness |
| SGLT2 inhibitors | e.g. dapagliflozin, empagliflozin — cardiorenal benefit concepts even without diabetes in many HF contexts | Genital hygiene, dehydration/hypotension risk, sick-day rules, rare euglycaemic ketoacidosis awareness |
Loop diuretics (furosemide, bumetanide) treat congestion and symptoms; they are essential for fluid overload but are not a substitute for disease-modifying pillars. Dose to the lowest effective amount that keeps the patient euvolemic when possible.
Fluid overload counselling
Community pharmacists reinforce the care plan between clinic visits:
- Daily weight at the same time of day; report rapid gains (e.g. several kilograms over a few days—use the patient’s written action plan thresholds).
- Salt awareness and fluid guidance as advised by the treating team (individualised; not a one-size slogan).
- Symptom watch: increasing ankle swelling, orthopnoea, nocturnal dyspnoea, reduced exercise tolerance, abdominal bloating.
- Adherence to all pillars and diuretics; explain that feeling “a bit better” is not a reason to stop disease-modifying therapy.
- Medicine review: NSAIDs, some calcium channel blockers (negative inotropes), and thiazolidinediones can worsen HF—flag for review.
Red flags — refer urgently
Do not optimise community packs alone when the patient is unstable:
- Acute severe dyspnoea, frothy sputum, or suspected acute pulmonary oedema
- Chest pain consistent with acute coronary syndrome
- Syncope, severe symptomatic hypotension, or new profound bradycardia on rate-limiting therapy
- Marked hyperkalaemia symptoms or laboratory crisis, anuria/oliguria with rising oedema
- Facial/tongue swelling suggesting angioedema
- Rapid weight gain with distress despite usual diuretic plan
Putting 3.2 and 3.3 together
Implement (3.2): select class-appropriate therapy, ensure combinations make pharmacological sense, counsel on how/when to take medicines, and explain expected adverse effects before they cause non-adherence.
Monitor (3.3): know which labs matter (K+, creatinine/eGFR), when cough or oedema is drug-related, when blood pressure or heart failure symptoms show under-treatment or decompensation, and when to escalate to the prescriber or emergency services.
Exam mindset
Typical items: ACEI cough management (switch strategy), “which monitoring after starting ramipril?”, triple-whammy AKI risk, HFrEF drug that should not be combined with ACEI (ARNI washout concept), spironolactone potassium risk, SGLT2 counselling point, or a breathless HF patient who needs referral rather than another OTC decongestant. Prefer answers that protect safety, monitoring, and disease-modifying therapy continuity over cosmetic blood-pressure tweaks alone.
A patient develops a persistent dry cough after starting perindopril for hypertension. Blood pressure is well controlled and there is no heart failure or infection. What is the most appropriate next step in most community scenarios?
Which monitoring pair is most characteristic after initiating or increasing an ACE inhibitor or ARB?
In HFrEF, which statement best reflects exam-level pillar therapy concepts?
A patient with known HFrEF presents to the pharmacy with sudden severe breathlessness at rest, inability to lie flat, and frothy sputum. What should the pharmacist prioritise?