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Diagnosis and management of acute heart failure

PRACTICAL THERAPEUTICS

 

Acute heart failure is a common reason for admission to hospital and is a medical emergency. This article focuses on the treatment options for the management of this patient group

 

Alison Warren BPharm(Hons) Dip Clin Pharm MSc (Cardiology)

Lead Cardiac Pharmacist,

Brighton and Sussex University Hospitals NHS Trust

Email: Alison.Warren@bsuh.nhs.uk

 

The European Society of Cardiology defines heart failure as “an abnormality of cardiac structure or function leading to the failure of the heart to deliver oxygen at a rate commensurate with the requirements of the metabolising tissues, despite normal filling pressures”.1

 

Acute heart failure is the rapid onset or change in the signs and symptoms of heart failure and is a life threatening condition requiring immediate medical attention. It is a leading cause of hospitalisation in people over 65 years of age. In the UK, the National Heart Failure Audit has been collating data on heart failure admissions since 2007. Although outcomes are improving, the prognosis is still poor with in-hospital mortality in the region of 10%, one-year mortality of 35–40% and a high probability of one or more re-admissions over the next 12 months.2

 

There are many causes of acute heart failure (Table 1), with decompensation of chronic disease, acute coronary syndromes (ACS) and ischaemic heart disease, cardiac arrhythmias, hypertension and valvular disease being the more common aetiologies. The clinical syndrome is characterised by a reduction in cardiac output, reduced perfusion of tissues and increased tissue congestion. This results in the myocardium being unable to maintain sufficient cardiac output to meet the demands of the peripheral circulation. Diagnosis and treatment are usually carried out in tandem, as treatments need to be imitated promptly.

 

Signs and symptoms

Many patients have significant volume overload and congestive symptoms will predominate: pulmonary oedema and shortness of breath associated with left sided failure and peripheral oedema, raised venous pressure with or without ascites with right sided failure (often a combination of the two). There will commonly be increased body weight, reduced urine output, fatigue and muscle weakness. There may be haemodynamic compromise with hypotension and poor tissue perfusion resulting in worsening renal function, hepatic dysfunction and cardiac compromise. In the most severe form the patient will be in cardiogenic shock. The New York Heart Association classification (Table 2) is used to describe the functional status of patients.

 

Diagnosis

The diagnosis is based on a summary of symptoms and the clinical findings and may be difficult. Initial investigations will include an ECG (rarely normal in heart failure patients) and a chest X-ray (cardiac size and the presence of pulmonary congestion may help to differentiate between cardiac and lung pathology). In addition to standard biochemical and haematological tests, it is also recommended to screen for thyroid disease and diabetes, to undertake baseline clotting parameters and to check cardiac enzymes to rule out an acute ischaemic event. 

 

More recently use of naturetic peptides (BNP or NT-proBNP) have been introduced with a single sample being used. These peptides are released from the cardiac ventricle in response to increased wall stretch and volume overload and have a high negative predictive specificity for heart failure.3 They do not confirm a diagnosis of heart failure but the following thresholds are used to rule out the diagnosis of heart failure: 

BNP less than 100ng/l

NT-proBNP less than 300ng/l

 

However, the gold standard tool for diagnosis is still the echocardiogram which is used to evaluate and monitor left and right ventricular function, valvular structure and function, pericardial pathology and mechanical complications of infarction thus directing the clinician to the aetiology and/or severity of the problem which in turn will direct the treatment plan. Ideally the results of an echocardiogram should be available within 48 hours of hospital admission.  

 

Goals of treatment

The immediate goals of treatment are to improve symptoms and stabilise the haemodynamic condition. Initially the main priorities are to achieve adequate oxygen levels and relieve distress. Subsequently treatments are given to reduce preload (volume returning to the heart) and afterload (the volume against which the heart pumps). Treatments will inevitably include diuretics and in selected cases vasodilators and/or inotropes. Reviewing the aetiology will determine whether there are any underlying correctable causes (for example, valvular disease, revascularisation of coronary disease, control of rhythm and/or rate disorders).  

 

Once the patient has been stabilised, careful initiation of the treatments for chronic heart failure will be required. The longer term management is beyond the scope of this article, but treatment of left ventricular systolic function in particular is guided by randomised controlled trials that form the basis of national and international guidelines.1,4

 

Pharmacological treatments for acute heart failure

Unlike chronic heart failure, in acute heart failure there is a lack of controlled clincial trial data to define the optimum treatment. The recommendations outlined below are drawn from the available evidence base and consensus expert opinion presented in published international guidelines.1,5

 

Oxygen 

Oxygen may be given to treat hypoxaemia (SpO2 <90%). Non-invasive ventilation can be used to improve oxygenation without the need for endotracheal intubation and therefore reduce the need for mechanical ventilation (which is reserved for patients who cannot tolerate the above or those who have respiratory muscle fatigue).

 

Opiates

Small bolus doses of opiates such as morphine are useful in patients who are particularly restless or agitated. Symptom relief results from a combination of venodilatation, mild arterial dilation and a reduction in heart rate thus reducing oxygen demand. 

 

Diuretics

It is clear from clinical experience that diuretics give rapid symptomatic relief of breathlessness and for fluid retention are still the mainstay of treatment. Diuretics increase urinary volume by increasing the excretion of water and sodium chloride resulting in reduction of the plasma and extracellular volume, reducing right and left heart filling pressures and relieving both peripheral and pulmonary congestion. Due to their relative potency, loop diuretics (furosemide, bumetanide) are the principal agents used. Initially the intravenous route will be required. However, despite their universal use the optimal strategy has not been determined. In a recent trial comparing 12 hourly bolus dosing with continuous infusions and low dose (equivalent to preadmission dose) with high dose (2.5 times the pre-admission dose) there was no difference in the primary endpoints. The high dose strategy did improve some symptomatic secondary endpoints but at the expense of transient worsening of renal function.6 Whatever strategy is used, doses need to be titrated with careful monitoring and are guided by signs and symptoms of fluid status with careful monitoring of renal function. In some cases achieving an adequate response may be difficult and several strategies have been suggested to improve diuresis/overcome diuretic resistance (Table 3).  

 

Mineralocorticoid receptor antagonists (MRAs)

An MRA (spironolactone or eplerenone) should be initiated/continued in patients with a reduced ejection fraction – providing renal function and potassium levels allow because these agents have been shown to offer a prognostic benefit. In particular eplerenone has evidence for use in the post-ACS population.10 In a more recent study in patients with heart failure with preserved ejection fraction, spironolactone had a neutral effect on outcome.11

 

Vasodilators 

Intravenous nitrates may be prescribed in specific circumstances for example concomitant myocardial ischaemia, severe hypertension or regurgitant aortic or mitral valve disease. Commonly dosage will be limited by low blood pressure and care should be taken to avoid hypotension (SBP <100mmHg).  Furthermore the use of nitrates is limited by the rapid development of tolerance and use should be restricted to periods of less than 24 hours. 

 

Inotropes

Inotropes may be required if there is severe reduction in cardiac output which may lead to end organ damage. Patients will generally be severely hypotensive and maybe refractory to diuretics and vasodilator therapy as outlined above.  

 

Dobutamine, usually the first choice agent, exerts its inotropic effects via the beta 1-adrenoreceptor. The positive inotropic effects improve cardiac output and consequently tissue perfusion and renal output. Blood pressure may increase slightly but more commonly little or no change is seen. Heart rate increases may be dose limiting particularly in patients with underlying atrial fibrillation. Other options include:

  • Phosphodiesterase inhibitors (milrinone or enoximone): inodilators 
  • Noradrenaline or adrenaline  
  • Dopamine at low dose (<3μg/kg/min). 

In some European countries the calcium sensitiser, levosimendan, is available. Trials involve a loading dose followed by a continuous infusion for up to 24 hours. The resultant haemodynamic effects are prolonged and continue beyond the duration of the infusion. In the early trials beneficial effects were seen compared to dobutamine however later studies did not show the benefits anticipated and the future development of this agent is unclear.12

 

Introduction of chronic therapy

Once the patient has stabilised in the acute phase it is important to consider the longer-term management. Every effort should be made to commence treatments for left ventricular systolic dysfunction during the hospital stay in line with the evidence base as this may have significant benefits in terms of mortality and morbidity.2 Where possible this should include the introduction and subsequent up-titration of both an ACE inhibitor (or an angiotensin receptor antagonist in cases of intolerance) and a beta-blocker licenced for the treatment of left ventricle systolic dysfunction in combination with an MRA and the lowest dose of loop diuretic required to maintain fluid status. Early follow-up in the outpatient setting is essential to enable close monitoring and to continue the optimisation of the evidence-based treatments. Pharmacists and heart failure nurses working in multidisciplinary teams are ideally placed to optimise medications for this patient group.1,13

 

Conclusions

Acute heart failure is a common cause for hospital admission. Prompt diagnosis and treatment is needed to ensure the patient is commenced on the right pathway of care. Pharmacological intervention is an important part of this treatment package and national and international guidelines exist to guide patient management. Ongoing management of these patients in line with guidelines for chronic heart failure is essential and has proven benefits in terms of both mortality and morbidity. Pharmacological interventions are the mainstay of treatment and this is a rewarding field where pharmacists can play an important role in medicines optimisation. 

 

Key points

  • Acute heart failure is a common reason for admission to hospital and is a life-threatening condition.
  • Echocardiogram is still the gold standard diagnostic tool.
  • Diuretics give rapid relief but need to be managed carefully to limit renal dysfunction.
  • Other treatment options include oxygen, opiates, vasodilators and inotropes.
  • Once stabilised, the management plan will involve introduction and up-titration of chronic heart failure treatments.

 

References

  1. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2102. The Task Force for the diagnosis and treatment of acute and chronic heart failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC. Eur Heart J 2012;33:1787–1847.
  2. British Society for Heart Failure. National Heart Failure Audit 2012–2013. www.ucl.ac.uk/nicor/audits/heartfailure/documents/annualreports/hfannual12-13.pdf (accessed 16 April 2015).
  3. Rutten FH. Naturetic peptide tests in suspected acute heart failure. A reliable tool for assessing acutely breathless patients. Br Med J 2015;350:h910.
  4. National Institute for Health and Care Excellence. Chronic Heart Failure: management of chronic heart failure in adults in primary and secondary care. Clinical guideline number 108, 2010. www.nice.org.uk/guidance/CG108 (accessed 16 April 2015).
  5. National Institute for Health and Care Excellence. Acute heart failure. Diagnosis and managing acute heart failure in adults. NICE clinical guidelines 187, 2014. www.nice.org.uk/guidamce/CG187 (accessed 16 April 2015).
  6. Felker GM et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med 2011;364:797–805.
  7. Jentzer J, De Wald T, Hernandez A. Combination of loop diuretics with thiazide type diuretics in heart failure. J Am Coll Cardiol 2010;56:1527–34.
  8. Costanzo M et al. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. JACC 2007;49:675–83.
  9. Bart B et al. Ultrafiltration in decompensated heart failure with cardio renal syndrome N Engl J Med 2012;367:2296–304
  10. Pitt B et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 2003;348:1309–21.
  11. Pitt B et al. Spironolactone for heart failure with preserved ejection fraction. N Engl J Med 2014;370:1383–92.
  12. National Institute for Health Research. Levosimendan (Leximda) for severe acute decompensated chronic heart failure. www.hsc.nihr.ac.uk/topics/levosimendan-leximda-for-severe-acute-decompen... line.
  13. McMurray J et al. Practical recommendations for the use of ACE inhibitors, beta-blockers, aldosterone antagonists and angiotensin receptor blockers in heart failure: putting guidelines into practice. Eur J Heart Fail 2005:710–21.

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