Add a suitable educational image showing the failing heart, pulmonary congestion and systemic perfusion here.
Why this topic matters: Heart failure is a clinical syndrome in which the heart cannot provide adequate output for the body’s needs, or can do so only at abnormally high filling pressures. Acute decompensation can deteriorate within minutes into pulmonary oedema, respiratory failure or cardiogenic shock. Emergency-care students must recognise congestion and hypoperfusion early, identify a reversible trigger, perform a structured ABCDE assessment, support oxygenation, use diuretics and vasodilators safely, avoid harmful routine fluid loading, and coordinate critical-care or cardiology escalation.
Learning objectives
- Define heart failure and distinguish chronic, acute, acute-on-chronic, left-sided, right-sided, biventricular, systolic and diastolic failure.
- Explain how reduced contractility, impaired relaxation, pressure/volume overload and neurohormonal activation produce congestion and low output.
- Recognise typical, atypical and life-threatening presentations, including acute pulmonary oedema and cardiogenic shock.
- Identify common precipitants using the CHAMPIT framework and obtain a focused OPQRST-SAMPLE history.
- Perform an ABCDE assessment, classify the patient as warm/wet, cold/wet, warm/dry or cold/dry, and communicate deterioration using SBAR.
- Describe the role and limitations of ECG, chest radiograph, natriuretic peptides, echocardiography, lung ultrasound, renal tests, troponin and blood gases.
- Outline pre-hospital, emergency-department, ward, high-dependency and critical-care management for acute decompensated heart failure.
- Explain safe use and monitoring of loop diuretics, nitrates, ACE inhibitors/ARBs/ARNI, beta-blockers, mineralocorticoid receptor antagonists, SGLT2 inhibitors, inotropes and vasopressors.
- Plan nursing observations, fluid balance, oxygen/NIV care, pressure-area care, medicine safety, patient education, discharge preparation and prevention of readmission.
1. Definition and core concepts
Heart failure (HF) is a complex clinical syndrome caused by a structural or functional cardiac abnormality that results in symptoms and signs from raised intracardiac pressures, inadequate cardiac output, or both. It is not simply “a weak heart”; a patient may have a normal ejection fraction but severe filling-pressure elevation and congestion.
| Term | Meaning | Emergency relevance |
|---|---|---|
| Heart failure with reduced ejection fraction (HFrEF) | Predominantly impaired left-ventricular systolic contraction; commonly EF ≤40%. | Often responds to guideline-directed disease-modifying therapy, but acute decompensation may require IV diuresis and ventilatory support. |
| Heart failure with mildly reduced EF (HFmrEF) | Intermediate systolic function, usually EF 41–49%, with clinical evidence of HF. | Symptoms and congestion can be severe despite a moderately reduced EF. |
| Heart failure with preserved EF (HFpEF) | Preserved EF with impaired relaxation, increased stiffness and raised filling pressures. | Often presents with hypertension, atrial fibrillation, obesity, renal disease or pulmonary oedema; EF alone must not reassure the team. |
| Left-sided failure | Left-ventricular or left-atrial dysfunction causing pulmonary venous congestion and reduced systemic output. | Crackles, hypoxaemia, orthopnoea and acute pulmonary oedema may develop rapidly. |
| Right-sided failure | Right-ventricular dysfunction or pulmonary hypertension causing systemic venous congestion. | Raised JVP, hepatomegaly, oedema, ascites and renal congestion; excessive fluids may worsen RV failure. |
| Acute decompensated HF (ADHF) | New or worsening HF symptoms and signs requiring urgent assessment or hospital treatment. | Look for hypoxaemia, shock, a trigger and end-organ injury immediately. |
| Cardiogenic shock | Primary cardiac pump failure causing inadequate tissue perfusion, usually with persistent hypotension or vasopressor need. | A resuscitation emergency requiring critical-care, cardiology and often revascularisation/mechanical support review. |
Safety principle: Ejection fraction is not a severity score. A patient with HFpEF can have life-threatening pulmonary oedema, while a patient with HFrEF may be chronically stable. Treat the clinical syndrome—congestion, perfusion, oxygenation and trigger—not a single number.
2. Causes and risk factors
2.1 Common underlying diseases
- Ischaemic heart disease and previous myocardial infarction causing scar, remodelling or recurrent ischaemia.
- Long-standing hypertension producing left-ventricular hypertrophy, stiffness and eventual systolic failure.
- Cardiomyopathies: dilated, hypertrophic, restrictive, arrhythmogenic, peripartum, inflammatory or toxic.
- Valvular disease, especially aortic stenosis, aortic regurgitation and mitral regurgitation or stenosis.
- Persistent tachyarrhythmia or bradyarrhythmia, including atrial fibrillation with rapid ventricular response.
- Congenital heart disease, pulmonary hypertension and chronic lung disease causing right-heart failure.
- Myocarditis, endocarditis, rheumatic valve disease and untreated infectious or inflammatory disease.
- Diabetes, obesity, chronic kidney disease, anaemia, thyroid disease and sleep-disordered breathing.
2.2 Precipitants of acute decompensation: CHAMPIT
| Trigger | Examples | What the emergency team should do |
|---|---|---|
| C – Coronary syndrome | Acute MI, unstable angina, stent thrombosis or ongoing ischaemia. | Obtain an urgent ECG and troponin, treat ACS according to protocol and involve cardiology early. |
| H – Hypertensive emergency | Severe afterload elevation, acute pulmonary oedema, aortic disease or renal crisis. | Repeat accurate BP, assess end-organ injury and use carefully titrated vasodilator therapy when prescribed. |
| A – Arrhythmia | AF with rapid rate, VT, severe bradycardia or heart block. | Continuous ECG, correct electrolytes and use synchronised cardioversion/pacing or rate/rhythm control when indicated. |
| M – Mechanical/valve problem | Acute mitral regurgitation, ventricular septal rupture, tamponade or prosthetic valve dysfunction. | Urgent echocardiography and specialist surgical/interventional review. |
| P – Pulmonary embolism | Acute RV strain, hypoxaemia or obstructive shock. | Assess VTE probability, obtain imaging if stable, and escalate reperfusion treatment if high-risk. |
| I – Infection/inflammation | Pneumonia, sepsis, myocarditis or endocarditis. | Take cultures when appropriate, start prescribed antimicrobials promptly and reassess fluid strategy carefully. |
| T – Tampering/non-adherence/toxins | Missed medicines, excess salt/fluids, NSAIDs, alcohol, cocaine/amphetamines or cardiotoxic medicines. | Ask without judgement, check the medicine list and address reversible exposure. |
2.3 Patient-level risk factors
- Previous HF admission, recent weight gain, reduced exercise tolerance or worsening orthopnoea.
- High salt intake, excessive fluid intake, poor access to medicines or inability to attend follow-up.
- Renal impairment, low haemoglobin, diabetes, thyroid disease or uncontrolled blood pressure.
- Pregnancy or the postpartum period, especially with hypertension or cardiomyopathy.
- Recent surgery, anaesthesia, blood transfusion, intravenous fluids, infection or immobilisation.
- Use of NSAIDs, corticosteroids, thiazolidinediones, some antiarrhythmics, negative inotropes or unregulated herbal medicines.
3. Pathophysiology
- A myocardial, valve, pressure or rhythm abnormality reduces effective forward flow or increases filling pressure.
- Reduced renal perfusion activates the sympathetic nervous system, renin–angiotensin–aldosterone system and vasopressin release.
- Tachycardia and vasoconstriction initially preserve blood pressure but increase myocardial oxygen demand and afterload.
- Sodium and water retention expand intravascular volume; increased preload raises pulmonary and systemic venous pressures.
- Interstitial and alveolar lung fluid impairs diffusion and compliance, causing breathlessness, hypoxaemia and respiratory fatigue.
- Chronic neurohormonal activation causes hypertrophy, fibrosis, ventricular dilatation and adverse remodelling.
- When compensation fails, cardiac output falls. Hypoperfusion causes cool skin, confusion, oliguria, lactic acidosis, renal injury and liver dysfunction.
- Right-ventricular failure reduces pulmonary blood flow and left-ventricular filling; excessive positive pressure or fluid loading may worsen output.
Clinical reasoning: Congestion and hypoperfusion can occur together. A patient with cold, wet HF needs urgent critical-care review; repeated fluid boluses may worsen pulmonary oedema, while diuresis alone may be dangerous if profound shock is present.
4. Classification for emergency practice
4.1 Left, right and biventricular failure
- Left-sided failure: pulmonary venous congestion, crackles, orthopnoea, pink frothy sputum, hypoxaemia and low systemic output.
- Right-sided failure: raised JVP, peripheral oedema, hepatomegaly, ascites, weight gain and congestive kidney dysfunction.
- Biventricular failure: combined pulmonary and systemic congestion with low-output features.
4.2 The four bedside haemodynamic profiles
| Profile | Bedside clues | General emergency priority |
|---|---|---|
| Warm and dry | Good perfusion, no major congestion. | Stable or compensated; investigate cause and optimise long-term care. |
| Warm and wet | Warm limbs with oedema, JVP elevation, crackles or pulmonary congestion. | Relieve congestion, monitor renal function and treat the precipitant. |
| Cold and dry | Cool limbs, narrow pulse pressure, fatigue or oliguria without obvious oedema. | Assess preload, shock and alternative causes; urgent senior review before diuresis or vasodilators. |
| Cold and wet | Poor perfusion plus pulmonary/systemic congestion. | High-risk decompensation; critical-care escalation, haemodynamic support and reversible-cause treatment. |
4.3 Functional limitation
- NYHA I: no limitation with ordinary activity.
- NYHA II: mild limitation; ordinary activity causes symptoms.
- NYHA III: marked limitation; less-than-ordinary activity causes symptoms.
- NYHA IV: symptoms at rest or inability to undertake activity without discomfort.
5. Clinical presentation
5.1 Symptoms of congestion
- Progressive exertional breathlessness, orthopnoea and paroxysmal nocturnal dyspnoea.
- Wheeze or cough, sometimes with pink or frothy sputum in pulmonary oedema.
- Rapid weight gain, ankle swelling, abdominal distension, early satiety or reduced appetite.
- Fatigue, reduced exercise tolerance, inability to lie flat and frequent night-time urination.
- Right-upper-quadrant discomfort from hepatic congestion or abdominal fullness from ascites.
5.2 Signs of congestion
- Tachypnoea, hypoxaemia, cyanosis, crackles, wheeze or increased work of breathing.
- Raised JVP, positive hepatojugular reflux, peripheral pitting oedema and sacral oedema.
- Third heart sound, displaced apex, murmurs, irregular rhythm or narrow pulse pressure.
- Hepatomegaly, ascites, pleural effusion, cool extremities or delayed capillary refill.
- Weight increase, reduced urine output, confusion, restlessness or inability to speak full sentences.
5.3 Red flags
Call for immediate senior/resuscitation help: severe breathlessness at rest; SpO₂ below the local target despite oxygen; inability to speak; exhaustion or silent chest; pink frothy sputum; systolic hypotension; new confusion or collapse; cold, mottled skin; urine output falling markedly; chest pain or dynamic ECG changes; sustained VT/bradycardia; or suspected cardiogenic shock.
6. Focused history: OPQRST-SAMPLE and CHAMPIT
| Question | Ask specifically | Why it matters |
|---|---|---|
| Onset and time | When did breathlessness, swelling, pain, weight gain or collapse begin? Sudden or gradual? | Separates pulmonary oedema, PE, MI, arrhythmia and chronic progression; time-stamps deterioration. |
| Provocation/palliation | Exertion, lying flat, night, salt/fluids, missed tablets, inhalers, oxygen, sitting upright? | Identifies orthopnoea, adherence problems and response to interventions. |
| Quality/region | Pressure, pleuritic pain, wheeze, cough, abdominal fullness, calf pain or palpitations? | Finds ACS, PE, infection, arrhythmia and competing diagnoses. |
| Severity/course | Number of pillows, walking distance, rapid weight gain, syncope, sleep disruption and change from baseline? | Quantifies functional decline and severity. |
| Associated symptoms | Fever, sputum, haemoptysis, chest pain, vomiting, diarrhoea, bleeding, dizziness or confusion? | Searches for CHAMPIT triggers and end-organ hypoperfusion. |
| Past cardiac history | HF type and EF, MI, hypertension, valve disease, cardiomyopathy, AF, devices, prior admissions? | Defines baseline risk and likely treatment response. |
| Medicine and allergy review | Diuretics, ACEi/ARB/ARNI, beta-blocker, MRA, SGLT2 inhibitor, anticoagulant, NSAID, last doses and allergies? | Prevents duplication, identifies non-adherence and medicine-related deterioration. |
| Social and practical history | Salt/fluid access, transport, caregiver support, finances, alcohol/stimulants, pregnancy possibility? | Supports safe discharge and identifies preventable readmission factors. |
7. Initial ABCDE assessment and triage
- Safety and help: place the patient in a monitored area, call emergency/cardiology/critical-care support, bring suction, oxygen, NIV equipment, defibrillator and IV access supplies.
- Airway: assess voice, patency, secretions and protective reflexes. Prepare airway support for exhaustion, reduced consciousness or impending arrest.
- Breathing: count respiratory rate, inspect effort and ability to speak, check SpO₂, auscultate, look for frothy sputum and use lung ultrasound if available.
- Circulation: measure BP in the correct cuff, pulse, rhythm, capillary refill, skin temperature, JVP, oedema and urine output. Establish IV access and draw urgent bloods without delaying treatment.
- Disability: assess mental status, glucose, agitation, confusion, syncope and fatigue. Hypoxia and low output may present as altered behaviour.
- Exposure: examine for oedema, sacral swelling, rash, infection, calf signs, medication patches, bleeding, pregnancy and signs of trauma while preserving warmth and dignity.
- Reassess frequently: document response after each oxygen, NIV, diuretic, vasodilator or vasoactive intervention. Trend rather than rely on one observation.
Positioning: Sit a breathless, normotensive patient upright with legs dependent when appropriate. If hypotensive or shocked, position according to perfusion and airway needs; avoid a rigid one-size-fits-all rule.
8. Investigations and interpretation
| Investigation | What it contributes | Nursing and safety points |
|---|---|---|
| 12-lead ECG and monitoring | Detects MI/ischaemia, AF, tachyarrhythmia, bradycardia, heart block, LVH and dangerous ventricular rhythms. | Obtain urgently, repeat with symptoms, attach monitoring and escalate dynamic changes. |
| Chest radiograph | Cardiomegaly, pulmonary venous congestion, oedema, pleural effusion, pneumonia or pneumothorax. | A normal film does not exclude early HF; do not delay life-saving stabilisation. |
| BNP or NT-proBNP | Supports or reduces the likelihood of HF in the appropriate clinical context. | Interpret with age, obesity, renal failure, AF, sepsis and timing; a result is not a substitute for examination. |
| Echocardiography | EF, chamber size, valve disease, wall motion, RV function, pericardial fluid and filling-pressure clues. | Urgent bedside echo is valuable in shock, suspected valve catastrophe or tamponade. |
| Lung ultrasound | B-lines, pleural effusion and lung sliding can support pulmonary congestion or alternative diagnosis. | Use with the clinical picture; pneumonia and ARDS can also produce B-lines. |
| Full blood count | Anaemia, infection and platelet count. | Anaemia can precipitate HF; thrombocytopenia changes anticoagulation/procedure safety. |
| Urea, creatinine and electrolytes | Renal perfusion, diuretic safety, potassium, sodium and magnesium status. | Report rising creatinine, severe dyskalaemia, hyponatraemia or oliguria promptly. |
| Troponin | Myocardial injury or ACS; chronic elevation can occur in HF and renal disease. | Use serial values and ECG; do not assume every elevation is type 1 MI. |
| Blood gas and lactate | Hypoxaemia, hypercapnia, acidosis and tissue hypoperfusion. | Use in severe distress or shock; monitor puncture site and do not delay escalation. |
| Urinalysis and liver tests | Proteinuria, infection, hepatic congestion or low-flow injury. | Trend changes and include in whole-organ assessment. |
8.1 Important differential diagnoses
- Acute coronary syndrome or mechanical MI complication.
- Pulmonary embolism, pneumonia, asthma/COPD exacerbation or pneumothorax.
- Renal failure with fluid overload, severe anaemia, sepsis or thyroid storm.
- Pericardial tamponade, acute aortic syndrome or myocarditis.
- Drug toxicity, high-output failure, panic or deconditioning.
9. Immediate and pre-hospital management
- Call emergency transport for severe breathlessness, syncope, chest pain, hypoxaemia, hypotension or suspected pulmonary oedema.
- Stop exertion, reassure and place the patient upright if perfusion allows. Do not let an unstable patient walk.
- Assess ABCDE, attach ECG and pulse oximetry, obtain serial BP and glucose, and establish IV access if trained and authorised.
- Give titrated oxygen for hypoxaemia or respiratory distress according to local targets; avoid routine high-flow oxygen in a well-saturated patient.
- Prepare CPAP/BiPAP for severe pulmonary oedema when the patient is conscious, protecting the airway and able to cooperate; monitor continuously.
- Bring the medication chart, last diuretic dose, allergies, kidney history, ECG, observations, onset time and fluid balance to the receiving team.
- Do not give repeated unmonitored fluid boluses to a congested patient; if shock is suspected, request senior haemodynamic guidance immediately.
10. Emergency-department management of acute decompensated HF
10.1 General goals
- Maintain airway and adequate oxygenation/ventilation.
- Relieve pulmonary and systemic congestion without causing renal or electrolyte injury.
- Restore adequate perfusion and protect brain, kidneys, liver and myocardium.
- Identify and treat CHAMPIT triggers.
- Reassess response frequently and decide early whether the patient needs ward, monitored bed, HDU or ICU care.
10.2 Oxygen and non-invasive ventilation
- Use the prescribed oxygen device and target saturation appropriate to the patient, including a lower target when chronic hypercapnic respiratory failure is known.
- CPAP improves alveolar recruitment and reduces work of breathing in cardiogenic pulmonary oedema; BiPAP may assist when ventilatory failure or fatigue is present.
- Check mask fit, pressure injury, vomiting risk, consciousness, BP, gas exchange and synchrony. Stop and escalate if the patient cannot protect the airway or deteriorates.
- Prepare for intubation and invasive ventilation when severe hypoxaemia, exhaustion, refractory acidosis, reduced consciousness or inability to tolerate NIV develops.
10.3 Diuretics
- IV loop diuretics are first-line for significant fluid overload or pulmonary congestion. Use the clinician-prescribed dose based on prior exposure, renal function and local protocol.
- Record time, route, urine output, weight, BP, renal function, sodium, potassium and magnesium. A poor response should prompt assessment of dose, absorption, renal perfusion, ongoing trigger and need for specialist escalation—not repeated blind doses.
- Watch for hypotension, dehydration, acute kidney injury, hypokalaemia, hyponatraemia, hypomagnesaemia, gout and ototoxicity with excessive or rapid dosing.
- Use a catheter only when clinically justified; measure hourly urine output in shock or critical illness and maintain a strict fluid balance chart.
10.4 Vasodilators
- IV nitrates may reduce preload and afterload in hypertensive pulmonary oedema when BP is adequate and no contraindication exists.
- Check BP before every titration; avoid or use extreme caution in hypotension, suspected RV infarction, severe aortic stenosis, recent PDE-5 inhibitor use or preload-dependent states.
- Document dose, response, headache, dizziness, reflex tachycardia and BP trend. A vasodilator is not a substitute for diuresis or treatment of the precipitant.
10.5 Medicines that require specialist direction
| Medicine/support | When considered | Important safety checks |
|---|---|---|
| ACE inhibitor/ARB/ARNI | Chronic disease modification and selected stable patients; not usually initiated or up-titrated during profound shock or acute kidney injury. | BP, renal function, potassium, pregnancy, angioedema and medicine interactions. |
| Beta-blocker | Continue in stable chronic HF unless shock, severe bradycardia, heart block or another contraindication; initiation/up-titration waits until stable. | Pulse, BP, perfusion, bronchospasm, conduction and signs of low output. |
| Mineralocorticoid receptor antagonist | Long-term HFrEF therapy in selected patients. | Potassium, creatinine, BP, dehydration and endocrine adverse effects. |
| SGLT2 inhibitor | Guideline-directed therapy in eligible HF phenotypes, including many patients with diabetes or CKD. | Volume status, renal function, genital infection, ketoacidosis risk and perioperative fasting. |
| Inotropes | Selected low-output shock with organ hypoperfusion under critical-care/cardiology supervision. | Continuous ECG, BP, ectopy, myocardial oxygen demand, lactate, urine output and extravasation. |
| Vasopressor | Persistent hypotension and shock after appropriate assessment, often norepinephrine in ICU protocols. | Arterial pressure, peripheral perfusion, rhythm, dose pump, central access policy and tissue injury. |
Do not use reflexively: Routine morphine, unmonitored fluids, high-flow oxygen in a well-saturated patient, NSAIDs, or rapid withdrawal of all chronic medicines. Each decision must match perfusion, congestion, renal function, BP and the local protocol.
11. Acute cardiogenic pulmonary oedema
- Call for help, sit the patient upright, attach ECG/SpO₂/BP monitoring and perform ABCDE.
- Give titrated oxygen for hypoxaemia and prepare CPAP/BiPAP if respiratory distress persists and there is no contraindication.
- Obtain ECG urgently; look for ACS, hypertensive emergency, valve catastrophe and arrhythmia.
- Give prescribed IV loop diuretic and, when BP permits, carefully titrated nitrate therapy.
- Check urine output, work of breathing, mental status, BP, renal function and electrolytes after each intervention.
- Escalate for intubation when NIV fails, consciousness declines, secretions cannot be managed or gas exchange remains unsafe.
- Search for trigger: infarction, AF with rapid response, infection, missed medicines, renal failure, excessive salt/fluids, stimulant use or acute valve disease.
12. Cardiogenic shock
Cardiogenic shock is inadequate tissue perfusion from primary cardiac dysfunction. Typical clues include persistent hypotension, cold clammy skin, narrow pulse pressure, confusion, oliguria, weak pulse, rising lactate, metabolic acidosis and pulmonary congestion. Normotension does not exclude early shock if vasoconstriction is maintaining BP.
| Priority | Actions |
|---|---|
| Recognise and call | Activate resuscitation, cardiology and critical-care teams. Use continuous ECG, frequent BP or arterial monitoring, pulse oximetry and strict urine output. |
| Find reversible causes | Urgent ECG/troponin, bedside echo, blood gas/lactate, electrolytes, chest imaging and assessment for MI, arrhythmia, tamponade, PE, sepsis or mechanical complication. |
| Oxygenation/ventilation | Give indicated oxygen and ventilatory support; avoid excessive intrathoracic pressure when it severely reduces venous return. |
| Fluids | Use only a cautious, reassessed fluid challenge when hypovolaemia or RV preload dependence is plausible. Stop if congestion or respiratory status worsens. |
| Perfusion support | Critical-care clinicians may use vasopressors and/or inotropes to maintain organ perfusion while treating the cause. |
| Revascularisation/mechanical support | ACS-related shock needs urgent revascularisation assessment. Selected refractory cases may require mechanical circulatory support where available. |
| Nursing surveillance | Trend mental status, skin, capillary refill, pulse, BP, lactate, urine output, fluid balance, access sites, arrhythmias and medicine adverse effects. |
13. Right-ventricular failure and special patterns
- RV failure may follow PE, RV infarction, pulmonary hypertension, severe lung disease or congenital heart disease.
- Signs include raised JVP, hepatomegaly, peripheral oedema, hypotension, clear lungs and low output.
- Large fluid loads can over-distend the RV and worsen septal shift; treat with specialist-guided preload optimisation and the underlying cause.
- Consider pregnancy/peripartum cardiomyopathy, myocarditis, renal failure, sepsis, anaemia and thyroid disease in younger patients.
- In pregnancy, involve obstetric, anaesthetic, cardiology and neonatal teams; balance maternal oxygenation and perfusion with fetal safety.
14. Chronic HF medicines and emergency reconciliation
| Group | Benefit | Emergency reconciliation and teaching |
|---|---|---|
| ARNI/ACE inhibitor/ARB | Reduces afterload, remodelling, admissions and mortality in selected HFrEF. | Check BP, potassium, creatinine, pregnancy and angioedema; never double a missed dose. |
| Evidence-based beta-blocker | Slows harmful sympathetic activation and improves survival in stable HFrEF. | Check pulse, BP, conduction and perfusion; do not initiate during acute shock. |
| MRA | Reduces aldosterone-mediated remodelling and admissions in eligible HFrEF. | Monitor potassium/renal function and teach avoidance of unapproved potassium supplements. |
| SGLT2 inhibitor | Reduces HF admissions and benefits many HFrEF/HFpEF patients, with or without diabetes. | Teach sick-day/perioperative advice according to local protocol; assess dehydration and ketoacidosis symptoms. |
| Loop diuretic | Relieves congestion and symptoms; dose is adjusted to volume status. | Daily weight, oedema, urine output, renal function and electrolytes; report rapid weight gain or dizziness. |
| Ivabradine/digoxin/other selected therapies | Specialist options for selected rate, rhythm or symptom problems. | Check pulse, renal function, toxicity signs and interactions; avoid self-adjustment. |
15. Nursing management and monitoring
15.1 Priority nursing observations
- Airway, respiratory rate, pattern, ability to speak, SpO₂, oxygen device, NIV tolerance and breath sounds.
- Pulse, rhythm, BP, capillary refill, skin temperature/colour, JVP, oedema and mental status.
- Strict input/output, urine output, daily weight, abdominal girth when relevant and fluid restriction adherence.
- Chest pain, orthopnoea, number of pillows, nocturnal symptoms, fatigue and activity tolerance.
- Laboratory trends: potassium, sodium, magnesium, urea, creatinine, haemoglobin, troponin and lactate.
- IV access, infusion pumps, diuretic response, vasoactive medicine effects and pressure areas from oxygen/NIV masks.
15.2 Interventions and rationales
| Intervention | Rationale and practical action |
|---|---|
| Position and oxygenate safely | Upright positioning and prescribed oxygen/NIV improve ventilation while reducing work of breathing; reassess BP and consciousness. |
| Maintain accurate fluid balance | Daily weight and input/output reveal congestion or over-diuresis earlier than oedema alone. |
| Administer medicines safely | Check the five rights plus renal function, BP, pulse, potassium, allergies and indication; document response and adverse effects. |
| Prevent skin and venous complications | Reposition, protect sacrum/heels, inspect oedematous skin and use prescribed VTE prophylaxis after arterial assessment. |
| Reduce myocardial workload | Cluster care, allow rest, avoid unnecessary exertion and treat anxiety without causing respiratory depression. |
| Escalate deterioration | Use SBAR with onset, trends, urine output, oxygen/NIV settings, medicines, ECG and response; do not wait for a routine round. |
| Support nutrition and function | Coordinate low-salt nutrition, appropriate fluid plan, renal/diabetes advice and physiotherapy; avoid malnutrition and unsafe deconditioning. |
16. Complications
| Complication | Warning signs | Priority response |
|---|---|---|
| Acute pulmonary oedema | Severe dyspnoea, crackles, frothy sputum, hypoxaemia and exhaustion. | Upright position, oxygen/NIV, diuretic/vasodilator orders, urgent senior review and airway preparation. |
| Cardiogenic shock | Hypotension, cold skin, confusion, oliguria, rising lactate and weak pulse. | Resuscitation/critical-care activation, echo, cause treatment and haemodynamic support. |
| Life-threatening arrhythmia | Palpitations, syncope, collapse, broad-complex rhythm or severe bradycardia. | Continuous ECG, defibrillator/pacing readiness and ALS protocol. |
| Acute kidney injury | Falling urine output, rising creatinine, electrolyte disturbance and fluid imbalance. | Review perfusion, medicines, diuretic response and renal/critical-care plan. |
| Thromboembolism | Sudden dyspnoea, chest pain, focal deficit or cold pulseless limb. | ABCDE, monitored transfer and PE/stroke/vascular pathway. |
| Hepatic congestion/low-flow injury | Jaundice, RUQ discomfort, rising transaminases, coagulopathy. | Treat haemodynamics and congestion; report trend. |
| Medicine/electrolyte toxicity | Weakness, cramps, confusion, hypotension, arrhythmia or severe diarrhoea. | Check potassium/magnesium/renal function and review medicines urgently. |
17. Discharge, education and prevention
- Explain the type of HF, precipitating event, medicines, monitoring plan and what each medicine is intended to do.
- Use teach-back: ask the patient to demonstrate weight recording, explain diuretic timing and state when to call for help.
- Provide a written safety-net: urgent care for breathlessness at rest, chest pain, fainting, confusion, blue lips, rapidly rising weight, markedly reduced urine or severe palpitations.
- Teach daily weight at the same time, symptom diary, prescribed salt/fluid plan and the action threshold agreed with the HF team.
- Encourage vaccination, smoking cessation, safe activity/cardiac rehabilitation, diabetes/BP control and avoidance of NSAIDs or unapproved herbal remedies.
- Confirm medicine supply, transport, caregiver support, follow-up, renal/electrolyte testing and access to emergency contact numbers before discharge.
- Review pregnancy plans, sexual health, work, mental health, health literacy and financial barriers sensitively.
18. Worked clinical scenarios
Scenario 1: Hypertensive pulmonary oedema
A 68-year-old with hypertension suddenly develops severe breathlessness, BP 220/120, crackles and SpO₂ 78%. The nurse calls for help, sits the patient upright, obtains ECG and monitoring, gives titrated oxygen, prepares CPAP and prescribed IV diuretic/nitrate therapy, and reassesses BP, work of breathing and urine output after each intervention. The team actively looks for ACS and arrhythmia rather than treating “fluid overload” alone.
Scenario 2: Cold and wet decompensation
A patient with known HFrEF is drowsy, cool, clammy, hypotensive and oliguric with crackles and raised JVP. The nurse recognises cold/wet HF, calls critical care, repeats ABCDE, obtains lactate and bedside echo, avoids unmonitored fluid boluses, prepares prescribed vasoactive support and communicates trends using SBAR.
Scenario 3: AF precipitant
A patient with oedema and orthopnoea has an irregular pulse of 160/min and fever. ECG confirms AF with rapid ventricular response. The team treats infection, assesses haemodynamic stability, corrects electrolytes, chooses rate/rhythm treatment safely and monitors for worsening pulmonary oedema; a negative inotrope is not given reflexively to an unstable patient.
Scenario 4: Discharge safety
A patient improves after IV diuresis but has limited transport and cannot afford all medicines. Before discharge, the nurse uses teach-back, confirms the next review and laboratory plan, checks the medicine supply, involves a caregiver with consent, explains warning signs, and documents a realistic follow-up plan. Clinical improvement without a safe plan is not complete care.
HEART-FAIL
H – Hypoxia and haemodynamics first · E – Examine congestion and end-organ perfusion · A – Assess CHAMPIT triggers · R – Relieve congestion safely · T – Track ECG, BP, urine and electrolytes · F – Find the phenotype: warm/wet or cold/wet · A – Avoid harmful routine fluids/NSAIDs · I – Initiate/continue evidence-based therapy when stable · L – Link discharge education, follow-up and prevention.
H – Hypoxia and haemodynamics first · E – Examine congestion and end-organ perfusion · A – Assess CHAMPIT triggers · R – Relieve congestion safely · T – Track ECG, BP, urine and electrolytes · F – Find the phenotype: warm/wet or cold/wet · A – Avoid harmful routine fluids/NSAIDs · I – Initiate/continue evidence-based therapy when stable · L – Link discharge education, follow-up and prevention.
19. Examination and revision questions
- Define heart failure and explain why a normal ejection fraction does not exclude severe acute decompensation.
- Differentiate left-sided, right-sided, biventricular, HFrEF and HFpEF presentations.
- Explain the neurohormonal response to reduced cardiac output and how it causes congestion.
- Use CHAMPIT to list and investigate precipitants of acute HF.
- Describe the ABCDE assessment for a patient with acute pulmonary oedema.
- Compare the warm/wet, cold/wet, warm/dry and cold/dry profiles.
- Discuss the roles and limitations of ECG, chest X-ray, BNP/NT-proBNP, echo, lung ultrasound and troponin.
- Outline safe nursing monitoring during IV loop diuretic therapy.
- When are oxygen, CPAP/BiPAP, vasodilators, inotropes and vasopressors considered?
- Why can repeated large fluid boluses worsen cardiogenic shock or right-ventricular failure?
- List at least six complications of acute HF and the warning signs that require escalation.
- Prepare a teach-back discharge plan for a patient recently admitted with acute-on-chronic HF.
Key takeaways
- Heart failure is a syndrome of congestion, inadequate output or both; ejection fraction alone does not determine urgency.
- Use ABCDE, continuous monitoring and the CHAMPIT trigger search at first contact.
- Warm/wet patients need safe decongestion; cold/wet patients need urgent critical-care and haemodynamic assessment.
- Oxygen is titrated to need; NIV can be life-saving in pulmonary oedema, but airway protection and BP must be monitored.
- Diuretics, nitrates, inotropes and vasopressors require repeated reassessment of BP, renal function, electrolytes, urine output and perfusion.
- Unmonitored fluid loading, NSAIDs, inappropriate high-flow oxygen and reflex medicine withdrawal can cause harm.
- Discharge education, access to medicines, follow-up and prevention are part of emergency care, not an optional afterthought.
Suggested references
- NICE. Acute heart failure: diagnosis and management (CG187).
- European Society of Cardiology. 2021 Guidelines for acute and chronic heart failure, with focused updates.
- AHA/ACC/HFSA. 2022 Guideline for the Management of Heart Failure.
- American Heart Association. Diagnosing heart failure and warning symptoms.
- American Heart Association. Medicines used to treat heart failure.
- Use current Uganda Ministry of Health, ambulance, emergency-department, cardiology and critical-care protocols for local medicine availability, referral and treatment targets.