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CDHB

Heart Failure

Definition

"Heart failure" is a pathophysiological syndrome, not a diagnosis, or a pathological process.

Management

Management requires each of the following:

• Recognition of the pathophysiological disturbance(s).
• Identification of the pathological process.
• Identification of precipitating cause(s).

Aetiology

Primary disease processes

• Ischaemic heart disease: myocardial infarction, ischaemic cardiomyopathy.
• Hypertension: systemic or pulmonary.
• Heart valve disease: especially mitral and aortic valve disease.
• Cardiomyopathy: dilated, hypertrophic, restrictive.
• Pericardial disease: constrictive pericarditis, tamponade.
• Congenital heart disease.
• High output states: cardiac beri-beri (alcoholics), Paget's disease, thyrotoxicosis, severe anaemia.

Contributing factors

The following are not generally the primary cause of heart failure but may exacerbate the physiological disturbance and therefore need to be considered when managing heart failure:

• Arrhythmias, particularly atrial fibrillation.
• Drugs:
  • Drugs with negative inotropic action such as beta-blockers, calcium antagonists, most antiarrhythmics.
  • Withdrawal of diuretics, ACE inhibitors, or digoxin, or poor compliance.
  • Fluid retention: steroids, NSAIDs, liquorice.
• Anaemia.
• Thyrotoxicosis - particularly in the elderly.
• Infections (especially endocarditis and pulmonary infections).
• Pulmonary embolism.
• Fluid overload - e.g., transfusion, renal failure.

Investigations

May be delayed while acute therapy is instituted and initial symptoms controlled.

• CXR (pulmonary venous congestion/oedema, cardiac size, pulmonary infiltrates).
• ECG (arrhythmia, ischaemia, acute or previous infarction).
• Myocardial injury markers: troponin and CK if the heart failure is acute or there has been a sudden deterioration.
• Na, K (urgently if ECG or rhythm abnormal), creatinine, Mg, Ca, PO₄.
• CBC.
• Echocardiography to assess LV function, valves, RV pressure estimate (urgent if hypotensive or if tamponade or bacterial endocarditis suspected).
• Thyroid function tests.
• ABGs if there is also COPD and there are concerns regarding CO₂ retention.
• Plasma BNP where there is doubt over cardiac vs non-cardiac cause of symptoms - refer to Guidelines for Use of BNP Measurements in an Acute Medical Setting.

  Note: It can take 4 hours for BNP to become abnormal if heart failure is acute.

Acute Heart Failure Therapy

Correct any contributing factors such as arrhythmia, infection etc.

• Always consider potentially reversible causes of severe heart failure (e.g., myocardial infarction, acute valvular regurgitation, pulmonary embolism) and institute appropriate therapy without delay.
• Acute pulmonary congestion, pulmonary oedema:
  • Sit patient upright.
  • Oxygen at 4-6 L/min only if the patient is hypoxic with a persistent sat.O₂ <92%.
  • Morphine 2.5 - 5 mg IV slowly over 3-5 minutes, count respiratory rate every 5 minutes. Care needed in patients with diminished level of consciousness and/or CO₂ retention.
  • Frusemide 40 - 120 mg IV - repeat as necessary to initiate diuresis. The effective dose will vary and the larger dose may be needed if patient is on frusemide maintenance treatment or has renal impairment.
  • Glyceryl trinitrate spray under tongue. Repeat doses of nitrate every 5 minutes while the blood pressure remains high.
  • If patient does not respond to initial treatment then nitrate infusion, continuous positive airway pressure (CPAP) by face mask, and haemodynamic monitoring in ICU or CCU should all be considered.
  • CPAP is useful if the patient remains breathless and hypoxia persists after initial treatment and may avert the need for intubation and mechanical ventilation. It is best started before the patient becomes severely fatigued. If prolonged therapy with high O₂ concentrations is required, consider other ventilatory supports.
  • In less distressed patients, oral frusemide may be sufficient but usually IV frusemide is required. Be alert to poor absorption from an oedematous GI tract in patients with chronic heart failure and peripheral oedema or ascites.
• Compromised myocardial function: Low output states can be managed by increasing myocardial contractility (inotropic support) or reducing the cardiac workload (pre load and after load reduction), and stopping negative inotropic agents.
• For patients in atrial fibrillation or flutter, consider digoxin.
  • Digoxin - indicated only for control of ventricular response in atrial fibrillation and atrial flutter in acute heart failure. It has value as a third line agent in chronic heart failure in sinus rhythm.
    • Give 0.5 mg digoxin initially (IV if in heart failure or nauseated).
    • Give further 0.25 mg increments every 4 hours to complete a loading dose of 1 mg. Elderly and renally impaired patients are prone to toxicity and may only require a total loading dose of 0.75 mg. Some younger patients may require a further two 0.25 mg increments to give a total loading dose of 1.5 mg. Assess clinically before giving each increment. Do not give a loading dose if recently on digoxin.
  • Consider maintenance dose of 62.5 micrograms to 250 micrograms per day.
  • Monitor clinically for efficacy. As with many drugs, plasma concentrations are poorly correlated to therapeutic effect.
  • In renal failure and the elderly reduce the maintenance dose.
  • Plasma concentrations may be used to monitor for suspected digoxin toxicity.
    • In atrial fibrillation, avoid concentrations >2 nmol/L.
    • In chronic heart failure, concentrations >1.5 nmol/L are associated with poorer clinical outcomes, with 0.7 - 1 nmol/L preferred.

Inotropic support:

• Intravenous adrenergic agonists are useful as short term emergency treatment in patients with severe heart failure on the basis of diminished myocardial function with low output and /or refractory congestion. They require ECG monitoring for arrhythmias and this can be done in CCU, Wards 12, 14, or ICU as necessary.

  Dobutamine* is probably the best drug to use for its positive inotropic effect as it causes little tachycardia and minimizes the increase in myocardial oxygen consumption. Place 500 mg (2 ampoules, each contains 250 mg in 20 mL) in 5% glucose to give a total volume of 500 mL (1 mg/mL) and run at 10 mL/hour (approximately 2.5 microgram/kg/min). Increase dose as required to achieve clinical response. Doses up to 10-15 microgram/kg/min can be used.

  If BP remains below 80 mm Hg systolic on dobutamine, a vasoconstrictor drug should probably be added (dopamine or adrenaline) to keep the BP above 80 mm Hg and thus maintain coronary perfusion. Give dopamine* (2.5-5 microgram/kg/min) by IV infusion. Can be increased up to 7.5-10 microgram/kg/min if necessary (2 hourly steps of 2.5 microgram/kg/min).

  *Caution: At Christchurch Hospital, the infusion details given here are used in CCU, but differ from those recommended by ICU.

• After load reduction:
  • In the acute situation, where oral therapy may not be suitable, use intravenous vasodilators such as glyceryl trinitrate or sodium nitroprusside. Nitroprusside will need close monitoring possibly including Swan Ganz and arterial pressure in CCU or ICU.
  • Correct any contributing factor such as arrhythmias, infection, etc.

Chronic Heart Failure Therapy

• Pre load reduction:
  • Nitrates, diuretics, morphine.
  • Fluid restriction is indicated in hyponatraemia, ≤1000 mL/24hr.
• After load reduction:
  • If BP well maintained use vasodilator therapy. Angiotensin converting enzyme (ACE) inhibitors are the treatment of choice. They can cause hypotension especially when given after intensive diuretic therapy and if there is hyponatraemia, therefore use with care. Aortic stenosis is a relative contraindication to ACE inhibitors but benefit will usually outweigh risk in established heart failure.
  • ACE inhibitor dosing: start with enalapril, quinapril or cilazapril. The dose modification for quinapril and enalapril in renal failure is given in the table below. For the Cockroft and Gault creatinine clearance formula, see Dose Alteration in Renal Impairment. The starting dose of cilazapril for a patient with normal renal function is 0.5 mg to 1.25 mg/day.

Side effects of ACE inhibitors include:

• Renal impairment: Reduce dose if creatinine rises and reassess diuretic dose provided heart failure is adequately controlled. Consider renal artery stenosis if creatinine has risen quickly.
• Hyperkalaemia: The need for potassium supplements is usually reduced.

• Spironolactone in low dosage (12.5-25 mg/day) has proven to be of benefit in heart failure when added to ACE inhibitors and loop diurectics. Careful monitoring of potassium and creatinine is required. Similarly, amiloride or triamterene are sometimes necessary to counter refractory congestion or loop diuretic induced potassium depletion. Potassium sparing diuretics should be used with caution if significant renal impairment and should not be combined.
• Thiazide diuretics (e.g., metolazone 2.5 mg once daily, bendrofluazide 2.5 mg once daily)
  • These agents can induce a profound diuresis in a patient with persisting oedema who is already on frusemide and a potassium sparing diuretic and can be extremely useful. They need to be given as a single 'one off' dose and their effect monitored.
• Further Management
  • Daily weight to monitor the effects of diuretic therapy. It is essential to have a baseline weight with which to compare.
  • Repeat CXR prior to discharge or if dyspnoea and/or clinical features fail to respond.
  • Consider echo in all new patients with a diagnosis of heart failure.
  • Consider echo if a pericardial effusion is suspected.
  • Low molecular weight heparin (enoxaparin 20-40 mg subcut q24h). Start on admission. Consider full heparinization then warfarin in those with chronic atrial fibrillation.
  • Potassium supplements will be needed with most diuretics. Requirements may be reduced or unnecessary in renal failure, with ACE inhibitor treatment, or when using potassium sparing diuretic therapy.
  • Re-evaluate the primary cause of the heart failure - attempt to confirm the primary disease process and exclude aggravating factors. This may include cardiac catheterization in selected cases.
  • Beta-blocker drugs do not have any role in the management of acute heart failure. However carefully titrated administration of beta-blockers reduces mortality in stable chronic heart failure associated with systolic dysfunction.

Guidelines for Use of Brain Natriuretic Peptide (BNP) Measurements in an Acute Medical Setting

• BNP is useful in distinguishing between cardiac failure and non-cardiac causes of dyspnoea in patients who are acutely unwell.
• In patients presenting acutely with new onset symptoms of breathlessness, where a diagnosis of heart failure is unclear (e.g., no clinical evidence, normal chest X-ray), a BNP of >120 pmol/L supports diagnosis of heart failure as the cause of breathlessness.

Notes:

• Normal range in healthy subjects is <30 pmol/L. In this situation, heart failure is unlikely.
• Values greater than 120 pmol/L suggest heart failure in a newly symptomatic (breathless) patient.
• In between these levels, heart failure is still possible, but all clinical information must be taken into account. BNP may be elevated by atrial fibrillation, LVH, valve disease, after myocardial infarction, in the elderly, and in severe renal impairment. BNP may be decreased by hypothyroidism, treatment with diuretics, vasodilators and ACE-inhibitors.
• Use of serial measurements to adjust therapy for heart failure rather than single tests for diagnosis can be useful to guide treatment.
• BNP does not add to the diagnosis in a patient with overt heart failure.
• BNP may be abnormal in patients with RV strain secondary to pulmonary hypertension.

Topic Code: 1307