CARDIOLOGY,  HeartFailure

Heart Failure – acute (APO)

Causes of acute decompensation of chronic heart failure
Acute myocardial ischaemia or infarction
Hypoxia (e.g., pneumonia, pulmonary embolism)
Arrhythmia (e.g., atrial fibrillation, ventricular tachycardia/ectopy)
Noncompliance with medications, fluid or salt restriction
Infection (e.g., respiratory, endocarditis, urinary, skin)
Pericardial tamponade
Anaemia
Receiving drugs that may worsen chronic heart failure
Hyperthyroidism or hypothyroidism
Adrenal insufficiency or corticosteroid excess
Increased sympathetic drive (e.g., phaeochromocytoma, Takotsubo cardiomyopathy, acute hypertension)
Mechanical catastrophe (e.g., ruptured interventricular septum, mitral papillary muscle or left ventricular free wall, or acute valvular regurgitation)
Acute renal failure

Medications that may cause or exacerbate heart failure
Centrally acting calcium channel blockers
Tricyclic antidepressants
Type I antiarrhythmic agents (e.g., flecainide, disopyramide and quinidine)
Corticosteroids
Thiazolidinediones (glitizones)
Tyrosine kinase inhibitors (e.g., sunitinib)
Saxagliptin
Anthracycline chemotherapeutic agents
Beta blockers, if used in unstable or unsuitable patients
NSAIDs (nonselective and COX-2 selective)
Clozapine
Drugs that prolong the QT interval
Moxonidine
TNF-α receptor antagonists (etanercept)
Trastuzumab (herceptin)
Minoxidil
Recreational stimulants (e.g., amphetamines or cocaine)
  • there are no guidelines or studies which specifically address the management of APO in the primary care setting. 
  • the goals of APo management are
    • symptom relief
    • reduction of extracellular fluid excess
    • improved haemodynamics
    • improved arterial oxygenation
    • satisfactory perfusion of the vital organS
  • General guidelines, approaches and goals must be modified according to clinical setting (eg. rural or metropolitan) and context (eg. APo in an elderly patient with end stage chF as opposed to a previously healthy patient 50 years of age).
  • the prerequisites for successful management of APo include appropriate:

• systems (triage, crisis resource management plans, organisation, leadership, teamwork, documentation)
• resources (personnel, equipment and drugs)
• knowledge and skills


Assessment, management and definitive therapy are concurrent, continuous and iterative. All patients require hospital admission for stabilisation and monitoring unless inappropriate, such as in the palliative care context. 

Assessment and management of acute pulmonary oedema

  • Initial • Call for help (other GPs, nurses, clinic staff, dial 000)
  • Commence oxygen
  • Insert 16 gauge intravenous cannula
  • Commence definitive treatment while assessing patient

History

  • Focused cardiorespiratory history (Note: nocturnal dyspnoea and orthopnoea are specific but not sensitive for heart failure)
  • Check past medical history, medications, compliance
  • Consider third party information

Examination

  • Five vital signs
    – temperature
    – pulse (rate, rhythm)
    – blood pressure
    – respiration (rate, pattern)
    – oxygen saturation
  • Focused cardiorespiratory examination, particularly:
    – colour
    – diaphoresis
    – jugular venous pulse
    – apex beat (shift, loading)
    – heart sounds (gallop rhythm?)
  • Murmurs (eg. mitral regurgitation, aortic stenosis)
    • Peripheral perfusion and oedema
    • Air entry, crepitations, rhonchi

Monitoring

  • Blood pressure
  • Continuous ECG (lead II) – if available
  • Oxygen saturation
  • Automated external defibrillator on standby
  • Consider urinary catheter if managing in rural hospital

Investigations (depending on availability)

  • 12 lead electrocardiogram (ECG) as soon as possible (APO is an acute coronary syndrome until proven otherwise)
  • Chest X-ray (portable, if available)
    • Signs of Pulmonary Oedema on Chest X-Ray
    • Bat-wing appearance – opacities extending laterally in a fan shape from each hilum
    • Kerley A lines – 5-10cm lines extending from the hila to the periphery (fluid in the deep septa)
    • Kerley B lines – 1.5-2cm lines seen in the periphery of the lower lung extending into the pleura (interlobular septal thickening)
    • Air bronchograms – tubular outlines of the smaller airways
    • Upper lobe diversion (cephalisation) – enlarged upper lobe vessels and smaller lower lobe vessels
    • Associated cardiomegaly (cardiogenic)
  • Point-of-care pathology tests (if available)
    • Troponin
    • B-type natriuretic peptide (BNP)
  • Other pathology tests: urea and electrolytes, liver function tests, glucose, urinalysis, full blood examination (FBE), arterial blood gases
  • Echocardiogram at earliest opportunity (depending on access and patient stability)
  • Reassurance and explanation
    • Patient and relatives

Clinical classification

Definitive Therapy for Acute Pulmonary Oedema

Therapy (Action)DoseNotes
PosturePatient supported in sitting up positionSupine position if unconscious or in cardiogenic shock
Oxygen10–15 L/min via Hudson type mask and reservoir bagInitial treatment even in patients with known COPD; monitor conscious state, respiratory rate, and oxygenation. When stable, reduce to 2–6 L/min via nasal prongs or 5–10 L/min via Hudson mask. For COPD, ideally use a 28% Venturi mask (flow rate 4 L/min). Titrate to achieve oxygen saturation of 94–96% (non-COPD) or 88–92% (COPD).
Glyceryl Trinitrate (Venodilator, reduces preload)400 µg sublingual every 5 minutes (up to three doses)Maintain systolic blood pressure (SBP) above 100 mmHg. Contraindicated within 48 hours of PDE5 inhibitor. For intravenous infusion, start at 10 µg/min and double infusion rate every 5 minutes according to clinical response (maintain SBP above 90 mmHg).
Positive Airway Pressure Support (CPAP or BiPAP)CPAP: 10 cmH₂O; BiPAP: inspiratory pressure 15 cmH₂O, expiratory pressure 5 cmH₂OReduces alveolar and pulmonary interstitial oedema; reduces venous return and preload. Contraindicated if SBP <90 mmHg or reduced consciousness. Clinical improvement may occur within 10 minutes. Duration depends on efficacy and tolerability.
Frusemide (Loop diuretic, reduces fluid overload; possible vasodilator effect)20–80 mg IV bolusAfter bolus, consider continuous IV infusion at 5–10 mg/hour (total dose <100 mg in first 6 hours, and <240 mg in the first 24 hours). Consider repeating a bolus dose after 30–60 minutes if no clinical improvement and no diuresis. Risk of hypovolaemia; avoid if no clear fluid overload.
Morphine (Reduces sympathetic nervous activity; possible venodilator effect)1–2 mg IVDoes not improve pulmonary oedema or cardiac output. Acts as an anxiolytic and reduces respiratory work.
Low Molecular Weight Heparin (Venous thromboembolism prophylaxis)Enoxaparin 40 mg SC dailyCommence if available.
Digoxin500 µg IV (over 5 or more minutes)Only for digoxin naïve patients with rapid atrial fibrillation.
Spironolactone25–50 mg orally statConsider in volume overloaded patients with poor response to IV frusemide.

Other Therapies That May Be Used in Intensive Care Unit

  • Adrenaline infusion
  • Vasopressin antagonists: Conivaptan, Tolvaptan
  • Vasodilators: Sodium nitroprusside
  • Inotropes (for cardiogenic shock or hypoperfused state with SBP <90 mmHg):
    • Beta-adrenergic stimulators: Dobutamine, Dopamine
    • Phosphodiesterase inhibitors: Milrinone, Enoximone
  • Ultrafiltration
  • Mechanical support (e.g., intra-aortic balloon pump) for cardiogenic shock

Oxygen Therapy in Acute Heart Failure

Monitoring

  • Recommended monitoring of peripheral arterial oxygen saturation in patients with acute heart failure.

Indications and Targets

  • Administer oxygen therapy if saturation drops below 94%.
  • Target oxygen saturation: 94–98%.
  • Lower target (88–92%) may be applied in those at risk of hypercapnia.

Opiate Therapy in Acute Heart Failure

Benefits

  • Helpful for venodilation and reducing respiratory drive and work of breathing.

Risks

  • Potential for excessive respiratory depression, hypotension, nausea, bradycardia.
  • Increased need for intubation.
  • Detrimental effects in acute MI and pulmonary oedema.

Recommendations

  • Anxiolytics and sedatives not recommended unless necessary to control agitation.
  • Generally avoid opiates in patients with hypotension, risk of aspiration, or hypoventilation.
  • Use opiates very cautiously in patients with uncontrollable agitation, with awareness of increased invasive ventilation requirement.

Diuretics in Acute Heart Failure

Indications

  • Recommended for patients with acute heart failure and congestion to relieve fluid overload symptoms.
  • First-line therapy for congestion indicators: pulmonary crepitations, peripheral oedema, elevated JVP, pleural effusion, hepatic congestion, ascites.

Administration

  • Administer only after establishing adequate perfusion and blood pressure.
  • IV diuretics preferred due to rapid action and effectiveness despite gastrointestinal hypoperfusion or bowel oedema.

Types and Dosing

  • Loop diuretics (e.g., furosemide [frusemide]) are the usual first choice.
  • Higher doses often needed in acute heart failure with congestion, may cause transient renal function deterioration.

Correcting the Cause

Cardiovascular Causes

  • Identify and manage myocardial ischaemia/infarction, uncontrolled hypertension, valvular disease, atrial fibrillation, tachycardia, pulmonary embolism.

Systemic Causes

  • Address infection, thyroid dysfunction, anaemia, poorly controlled diabetes, previous chemotherapy/radiotherapy, peripartum cardiomyopathy.

Idiopathic or Genetic Causes

  • Manage conditions like dilated cardiomyopathy, hypertrophic obstructive cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy.

Alcohol and Substance Abuse

  • Consider and manage issues related to alcohol and substance abuse (e.g., amphetamine).

Comorbid Diseases

  • Recognize and address comorbid diseases that worsen heart failure or complicate its treatment.
  • Particular attention to renal dysfunction (cardiorenal syndrome), which has a poor prognosis.

Postacute Care

Structured Management Plan:

  • Define problems, goals, and actions with patient and GP.
  • Utilize Medicare primary care items where applicable.

Team-Based Care:

  • Involve necessary healthcare professionals:
    • GP
    • Practice nurse
    • Cardiologist and/or heart failure clinic
    • Pharmacist
    • Aboriginal health worker
    • Dietician
    • Exercise physiologist

Education and Support:

Home Assessment and Community Support:

  • Ensure adequate support at home and in the community.

Patients

  • Ongoing education about self-management 
  • heart failure action plan
    • self monitoring (symptoms, weight, BP)
    • Should know the weight at which their condition was previously stable. 
    • They need to monitor their weight regularly so that they and their caregivers are alert to any weight gain which would suggest fluid retention. 
  • Smoking Cessation
  • Diet: Follow Heart Foundation guidelines, no added salt.
  • Fluid Restriction: Maximum 2 L/day (1.5 L/day if severe CHF).
  • Alcohol: No more than one unit per day.
  • Exercise: Develop an individualized program.

Investigations:

  • Echocardiogram: Mandatory for all patients post-AHF.
  • Full Cardiac Workup:
    • ECG
    • Lipid profile
    • Glucose
    • Renal function
    • Liver function
    • Thyroid function
    • Iron studies
    • Full blood examination (FBE)

Monitoring:

  • Patient Self-Monitoring: Symptoms, weight, blood pressure.
  • GP Review: Frequency determined by severity and stability of CHF.
    • Review symptoms, weight, BP, cardiorespiratory status.
    • Manage risk factors and comorbidities (e.g., ischaemic heart disease, diabetes, COPD, renal impairment, sleep apnoea, obesity, depression, osteoarthritis).
    • Assess mental state.
    • Conduct medication review (Medicare primary care items may apply).
    • Check pathology (urea, creatinine, electrolytes, FBE).

Medications Indicated:

  • ACE Inhibitor (ACEI): All patients with CHF (*improves prognosis and symptoms).
    • Use angiotensin II receptor blocker if ACEI not tolerated.
  • *Beta Blocker: Patients with systolic failure; COPD is not a contraindication.
    • Options: bisoprolol, carvedilol, metoprolol, nebivolol.
  • Frusemide: For symptoms of fluid overload.
  • Spironolactone: Add on if symptom control is inadequate (*improves prognosis).
  • Digoxin: Consider for atrial fibrillation or as add-on therapy for sinus rhythm with severe CHF inadequately controlled with the above.

Medications Contraindicated or Cautioned:

  • Contraindicated:
    • Verapamil
    • Diltiazem
  • Caution:
    • NSAIDs or cyclo-oxygenase-2 inhibitors
    • Corticosteroids

Vaccinations:

  • Influenza
  • Pneumococcal

Device Therapy (for moderate or severe CHF):

  • Cardiac Resynchronization Therapy: Consider if QRS is greater than 120 ms.
  • Implantable Cardioverter Defibrillator: Cardiologist to assess and recommend if appropriate.

Leave a Reply

Your email address will not be published. Required fields are marked *

This site uses Akismet to reduce spam. Learn how your comment data is processed.