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Heart Failure

Introduction

Heart failure (also CCF – congestive cardiac failure) is a clinical syndrome which refers to a state of reduced cardiac output. Typically it is defined as:

The inability of the heart to pump adequate amounts of blood to meet the body’s metabolic demands

This can be due to an inability for the heart to fill will blood correctly, or an inability of the heart to eject blood effectively.

Heat failure is the end stage of many cardiac diseases. It is a serious condition with a high rate of mortality and morbidity. 50% of patients will die within 5 years of diagnosis. The annual mortality rate is 10%, and 50% for those with severe heart failure.

Studies show that heart failure is chronically under treated. It accounts for 5 in 1000 hospital admissions each year in the UK.

It is a relatively common disorder which affects about 1-2% of the population.

The classical presentation includes shortness of breath (especially on exertion and on lying flat), fatigue and ankle oedema. Signs may include hepatomegaly, tachycardia, tachypnoea and raised JVP.
Historically diagnosed clinically (without the need for investigations) with the Framingham Criteria, although more recent guidelines from the European Society of Cardiology require the presence of signs and symptoms of heart failure, with “objective evidence” (usually an echocardiogram).

ACE-inhibitors are the mainstay of treatment and have been shown to increase survival. In the acute presentation with fluid overload, diuretics (particularly frusemide) and GTN are used. B-blockers can improve systolic function in cases where it is impaired. Other drugs that may be considered include digoxin, where atrial fibrillation is a contributory factor, and spironolactone may be added additional to frusemide for symptomatic patients.

The exact drug choices will be influenced by the specific features of the individual case.

Controlling other risk factors and co-morbidities can also prolong survival, for example;

Terms

There are many terms used in the description of heart failure. In the specialist setting, defining the specific type of heart failure may have an impact on the management (e.g. certain drugs will be more effective in different types of heart failure).

Epidemiology

The prevalence of heart failure is increasing. This is thought to be due to the ageing population and better survival in patients with cardiovascular disease.

Causes of Heart Failure

Heart failure is the end-point for almost all cardiac disease. Identifying the underlying cause is important, because treating it can prevent the progression of heart failure.

Pathophysiology

MAP – Mean Arterial Pressure
CO – Cardiac Output
TPR – Total Peripheral Resistance
SV – Stroke Volume
EDV – End Diastolic Volume
ESV – End Systolic Volume
HF causes a drop in MAP that initially stimulates baroreceptors that feed back into the medullary cardiovascular center [MCVC]. MCVC tries to increase and maintain the MAP by reducing vagal tone and increase sympathetic tone leading to increase heart contractility and rate therefore output. The sympathetic system also stimulates the contraction of arteries [increasing TPR] and veins [increasing venous return] and the release of adrenaline from adrenal medulla, which stimulate all of the above actions. The renin-angiotensis-system [RAS] is also stimulated in heart failure due to reduced kidney perfusion caused by reduced MAP and vasoconstriction and direct sympathetic stimulations. The end product, Angiotensin II, causes vasoconstriction, aldosterone release and ADH release causing sodium and water retention by the kidneys. These mechanisms are beneficial initially as they increase blood volume, therefore venous return and SV, TPR and HR, therefore maintaining a high CO, however, chronically these compensatory mechanisms act to worsen the situation;

Increase TPR

Increase HR

Fluid retention

Clinical presentations

Symptoms
Symptoms of Heart Failure
Signs
Elevated JVP
Pitting Oedema

Diagnosis

Guidelines about the diagnosis of heart failure vary. Traditionally it was a clinical diagnosis (see Framingham Criteria below), but in recent years, this has been superseded by the use of echocardiography. Most guidelines now recommend a combination of clinical suspicion and echocardiography to confirm the diagnosis.

The Framingham Criteria

A formal set of diagnostic criteria for congestive heart failure (CHF) resulted from the well-known Framingham Heart Study (an excellent example of a prospective study, to be mentioned in any public health examinations!). As with other diagnostic criteria systems this one makes use of Major and Minor criteria which, apart from being study aids in themselves, are sure to impress finals examiners if you can remember them (mnemonics provided for this purpose).

Diagnosis of congestive heart failure using the Framingham criteria requires simultaneous presence of 2 Major or 1 Major and 2 Minor criteria, which provide for a 100% sensitivity (but 78% specificity) value when diagnosing the symptoms and signs of CHF.

Small print is that the Minor criteria can only be used if they are not attributable to other medical conditions (eg. pleural effusions cannot be due to infection, malignancy, etc).

One set of mnemonics for the criteria is the following: SAW PANIC for the Major, and HEART ViNo for the Minor. Although, there are probably infinite other (less tame) personalized mnemonics out there!

Investigations

The single most useful investigation is echocardiogram. However, this is not always practicable or timely to access. Initially all patients should have an ECG and CXR, and in the UK, BNP.

ECG

CXR

CXR Signs in Heart Failure

BNP (B-type natriuretic peptide)

Other Blood Tests

  1. FEB – for anaemia
  2. U+E for Hyponatremia [in severe disease due to dilution] and Hypokalemia / Hyperkalemia
  3. LFT’s to detect extent of liver congestion/damage
  4. TFT’s to rule out thyrotoxicosis or myxedema
  5. HbA1c to check for co-existing T2DM

Echocardiogram

Angiography – can be used to assess the extent of IHD
Pulmonary function tests – to exclude lung disease causing breathlessness

Classification of Heart Failure

New York Heart Association [NYHA] Classification of Heart Failure. One year mortality in brackets

Prognosis

Survival Rates (%) for comparison with heart failure
Time from Dx
1 Year
2 Years
5 Years
Heart Failure
67
41
24
88
80
72
75
64
55
56
48
42

Complications of HF

  1. Muscle underperfusion causing muscle weakness and atrophy causing fatigue, exercise intolerance and dyspnea
  2. Increase risk of thromboembolism and stroke development. This is due to blood stasis, arrhythmias and existing atheromas.
  3. Arrhythmias – arrhythmias are associated with HF and are responsible for a large proportion of death in patients with HF. Arrhythmias usually results from increase in fibrous tissue deposition during tissue remodelling post-insults. Arrhythmias themselves lead to HF therefore they worsen the situation when they exist. AF is the most common atrial arrhythmia that co-exists with HF and is associated with increased risk of thromboembolism and stroke development. Ventricular Tachycardia [VT] is common in advanced HF, which may evolve into ventricular arrhythmias and cardiac arrest. Beta-blockers treatments are used to minimize these VT, hence sudden death
  4. Increased risks of infections that can initiate an acute-on-chronic event

Management

All those suspected of heart failure should be referred to a cardiologist for specialist management. In the meantime, treatment can be initiated in the community (or in the emergency department if an acute presentation). Below, we first discuss chronic, and then emergency management.

Non-pharmacological interventions

Pharmacological intervention

Most patients with class I and II disease will be treated with an ACE-i and a diuretic. More severe cases may require additional medications. The choice of beta-blocker and calcium channel blocker is particularly important, as some can worsen prognosis and clinical features.

Typically, patients start on low doses and the dose is titrated upwards to effect over several weeks.

A(ACE-i), B(b-blocker), C(Ca blockers and vasodilators), D(diuretics, digoxin)

ACE inhibitors [ramipril, enalapril, lisinopril, captopril]

Other vasodilators

Beta-blockers [e.g. atenolol, bisoprolol, carvedilol]

Diuretics

Digoxin; considered in;

Amiodarone in arrhythmic patients

Calcium channel blockers

Angiotensin receptor neprilysin inhibitors (ARNI)

A stepwise approach

Heart transplant may be considered where facilities are available for patients with significant heart failure.

Drugs to avoid

Improve Prognosis
Improve Symptoms (but not prognosis)
ACEi
Cardioselective β- blockers (β1)
E.g.  atenolol, bisoprolol, carvedilol
Angiotensin-II receptor antagonists
Spironolactone
  • Loop diuretics
  • Digoxin
  • Vasodilators – e.g. nitrates, hydralazine

Surgical intervention

Implantable devices

  • Pacemaker
    • Biventricular pacemakers are useful in patients with heart failure and bundle branch block
  • ICD – implantable cardiac defibrillator
    • Recommended in patients with an ejection fraction of <35% or those with a previous cardiac arrest
  • Left ventricular assist device (e.g. VentrAssist)

Diastolic heart failure

  • Has a different treatment – aim for inotropic effect
  • Use calcium channel blockers early – often in combination with beta-blockers
  • Avoid use of diuretics and strong vasodilators as these can worsen the condition – sometimes catastrophically due to decreased cardiac output
  • ACE inhibitors are only sometimes used – and with caution

Common pitfalls in management

  • Overuse of diuretics
  • Use of diuretics as a monotherapy – without use of an ACE-inhibitor
  • Failure to treat underlying causes
  • Failure to monitor electrolytes and renal function

Emergency management

HF can present acutely as acute HF or acute-on-chronic HF

Acute HF
Usual clinical presentations are dyspnea, anxiety and tachycardia. Acute HF can evolve into cardiogenic shock, which is an acute circulatory failure due to improper/inappropriate fluid distribution. Pallor and Hypotension [systolic <90], reduced CO and oliguria characterize cardiogenic shock. SHOCK CAC
Acute HF usually results from an acute event such as MI, arrhythmias, mechanical disease [valve rupture], pericardial disease etc…
Management involves;

In advanced situation can consider;

Acute-on-Chronic HF

Flashcard

References

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