Heart Failure

NB This post mainly deals with left sided heart failure.

The inability of the heart to supply the circulatory needs of the body despite an adequate circulatory volume.

Background and Epidemiology

• Not uncommon- particularly in the aging population
  • Incidence/prevalence increases with age
    • 1% of people 45-64 years old; 3% of people 65-74; 7% of people 75-84; 20% of people 85+
  • More common in men stratified by age; more common in women overall
  • 6 month mortality can be as high as 15% and 5 -year mortality up to 50%
• Classifying Heart Failure
  • Can be classified as new-onset (acute or slow-onset), transient (recurrent or a single episode) or chronic (whether stable or progressive)
  • Can also (technically) be classified by systolic or diastolic failure.  However, the majority of patients will have some degree of both.
    • Left ventricular systolic dysfunction is a common feature of systolic failure
      • Often defined as a LV ejection fraction of <40% on echocardiography
    • Some patients have normal LVEF (can be known as diastolic HF; HF with preserved LV function; HF with a normal ejection fraction (HFNEF) or HF with preserved systolic function (HFPSF)
  • Finally, heart failure can be classified as either
    • high output- where the problem is not necessarily with the heart but the systemic circulation.  Conditions like chronic anaemia, sepsis, hypercapnia, hyperthyroidism, pregnancy, arteriovenous shunting etc will increase cardiac output to levels outwith the capacity of the heart (resulting in features of heart failure)
    • low output- classical heart failure where dysfunction of the heart is the problem.

Pathophysiology and Causes

• Normal
  • Output = stroke volume × heart rate
    • Normally = 0.06-0.1 (l per beat) × 60-100 (bpm) = 3.6-10l/min.  NB Normally range is referred as 4-8l/min
    • SV is affected by 3 factors
      • preload- the amount of myocardial fibre stretch at the end of diastole
      • afterload- the resistance that must be overcome in order for the ventricle to eject blood
      • contractility- the ability of the heart to contract for a given afterload and preload
• Common causes of heart failure:
  • Contractile impairment e.g. Ischaemic heart disease (ACSs or chronic disease e.g. angina) (common)
  • Increased pressures e.g. Hypertension (most common); valvular disease e.g. aortic stenosis
  • Volume loading e.g. valvular disease e.g. aortic or mitral regurgitation
  • Diabetes
  • Restricted filling e.g. restrictive pericarditis; Hypertrophic cardiomyopathy (NB these tend to be causes of diastolic heart failure)
  • Congenital heart disease
  • Drugs (chemotherapy, calcium channel blockers or beta blocker overdose, illicit drugs e.g. cocaine)
  • Dysrhythmias e.g. severe tachy- or bradycardia
• Pathological and physiological compensatory mechanisms
  • Frank-Starling Mechanism
    • In the normal individual, this is a normal and useful homeostatic physiological response which allows the cardiac output to respond to changes in venous return
      • Increased venous return increases the ventricular filling (end-diastolic volume) and therefore increases the preload (initial stretch of myocytes).  This increases the force generated by the myocytes and thus increases SV and CO.

NB Cardiac output should actually be Stroke volume, as this curve is independent of heart rate.

• In heart failure, the heart (usually) has less contractility and so cardiac output is reduced to begin with.  Furthermore stroke volume only increases a little in response to larger increases in EDV.
• In the early stages of heart failure, the body will try and overcome this by increasing the preload and utilising the Frank-Starling mechanism.
  • Unfortunately, this increase in preload means that the heart has to work a lot harder with increased end-diastolic volumes, increased heart rate and increased afterload.
  • As heart failure progresses (see below), the ability of the heart to compensate is lost (line flattens) and even reverses.  It is at this point that the EDV is transmitted back through the left ventricle into the lungs, resulting in Po Oedema.
• Compensatory Mechanisms
  • Neurohormonal Activation
    • Again, another normal physiological response involved in maintaining mean arterial pressure (CO×TPR).
      • Normally, these mechanisms will be transient, e.g. in injury/exercise etc
      • In heart failure, they are constant and chronic
    • A decrease in MAP activates the sympathetic nervous system and release of catecholamines e.g. noradrenaline and adrenaline.
      • Increases HR and contractility (raising SV)
      • Increases vasoconstriction (increasing TPR)
      • Prolonged activation can lead to worsen heart failure, increasing ischaemic damage due to increased heart rate and promoting ventricular hypertrophy and arhythmias.
    • Direct reduction in renal blood pressure, as well as sympathetic activation, also activates the renin-angiotensin-aldosterone system
      • This induces sodium and water retention, increasing the pre-load and thus increasing myocardial energy expenditure
      • (angiotensin II is also thought to cause apoptosis of cardiac myocytes)
  • The problem is that normally, these processes are transient/episodic.  In heart failure, they are constant/chronic, and eventually lead to ventricular remodeling.
• Ventricular remodeling
  • Initial changes are compensatory.  There are several different patterns of remodeling:
    • Concentric hypertrophy (usually caused by an increased pressure load).
      • Initially increases contractility and CO but this muscle wall eventually stiffens (usually due to a failure to relax contraction- which is in turn due to the sympathetic response and hypertrophy)
    • Dilated cardiomyopathy (can be a sequela to hypertrophic remodelling or occur on its own)
      • Initially, an increase in chamber size can increase the pre-load and thus CO.  However, thinning of the ventricular wall also occurs.  The overall result is a reduced systolic function.
        • This may also cause atrioventricular valve regurgitation and/or conduction abnormalities (commonly LBBB)
          • This branch block can further worsen problems as it can cause regional delays in ventricular contractions (one area finishes whilst another is still contracting)
            • mechanical dysfunctions
• The role of Natriuretic peptides
  • Natriuretic peptides are released by the heart in response to wall stretch when there is circulatory volume expansion
    • ANP is predominantly released from the atria and BNP from the ventricles
  • Act on the kidney tubule to promote natriuresis (sodium excretion) and on the peripheral vasculature to promote vasodilation
    • I.e. they antagonise the effects of the RAA-system
  • It is thought that, in heart failure, ANP/BNP fail to compensate for activation of RAAS
    • BNP can be a good diagnostic and prognostic marker in HF (high levels at diagnosis suggest a poorer outcome)
• Inflammation is also now thought to play an important role in the pathogenesis of heart failure.

(for more information on the pathophysiology of heart failure, check out these 2 articles here and here)

Presentation

• History
  • Predominant symptom is shortness of breath.  Onset is gradual and may occur after a previous MI.  (Always ask about previous heart disease- congenital or acquired)
    • Dyspnoea and fatigue, particularly with exertion (the degree of exertion is important- as it can be minimal)
    • Orthopnoea
    • Paroxysmal Nocturnal dyspnoea
    • Dyspnoea at risk
  • The patient may describe chest pain with the shortness of breath
    • Usually described as a pressure across the chest (may be difficult to distinguish between this and myocardial infarction)
    • Palpitations may also be present
  • Other symptoms include
    • nocturia and oliguria
    • nocturnal cough/wheeze (this may be productive of pink/frothy sputum- important to ask about)
    • peripheral swelling/oedema (can be marked- e.g. up to the thigh)
    • Weight loss, muscle wasting and fatigue are usually seen later on in disease
  • Make sure to ask about presence of risk factors e.g. CVS disease, age, diabetes, hyperlipidaemia, hypertension
• Examination
  • Generally, the patient may appear unwell/short of breath; they may have cool peripheries; a tachycardia; in overt heart failure, patients are usually hypotensive (patient may be hypertensive early on in the disease)
  • The patient may have a raised JVP
  • A prominent second sound and the third heart sound may be heard (often termed a ‘gallop rhythm’- sounds immediatly after S2 and is often similar in sound or quieter- due to blood ‘sloshing’ around in the ventricles during early diastole)
  • Pulsus alternans is a term used to describe alternating strong and weak pulses.  This can occur in heart failure- it indicates a poor prognosis
  • There may be bilateral basal end-inspiratory crackles
  • There is usually some leg oedema
  • There may be other signs (less common) e.g.
    • Hepatomegaly
    • Pleural rub (effusion)
    • Ascites

Classification of Severity (New York Heart Association)

1. Patients with disease but resulting in no limitation of physical activity.
2. Patients with cardiac disease resulting in slight limitation of physical activity (comfortable at rest, but physical activity results in fatigue, palpitations, dyspnoea or anginal pain)
3. Patients with disease resulting in marked limitation of physical activity (comfortable at rest but minor activity causes symptoms)
4. Patients with disease resulting in inability to carry out any physical activity without discomfort (symptoms may be present at rest)

Investigations (according to guidelines)

• For patients with suspected heart failure, basic tests should be investigated, including
  • FBC, U&Es (measure renal function and CK), Glucose
  • Urinalysis
  • TFTs
  • ECG- may show tachycardia, LBBB
  • CXR- look for signs of heart enlargement (>33% of the width of the chest)
    • In the acute setting, there may also be pulmonary oedema which can be superacute (flash/batswing) or subacute (appear as Kerley B line/fissure fluid collections)
• If the patient does NOT have a history of previous MI (/CVD), measure serum BNP (brain natriuretic peptide)
  • If these are normal/low (<100pg/ml) (+ in keeping with other investigations)- HF unlikely
  • If they are high/raised (>400 or 100-400pg/ml) (or the patient DOES have a PMHx of cardiovascular disease (MI))- perform Doppler Echocardiography
    • Look at cardiac function (particular estimated left ventricular ejection fraction)
      • NB- remember that if the patient has normal ejection fraction this does not preclude the diagnosis of heart failure (HF with a normal ejection fraction is a clinical diagnosis)
• You may also want to check lung function with spirometry, peak flow etc

Management

• Lifestyle
  • Smoking cessation
  • Alcohol advice
  • If obese/overweight, consider weight loss; if cachexic, consider dietitian referral
  • Low salt diet (<3g/day)
• It may be appropriate to fluid restrict patients with HF 
• Pharmacological management
  • If LV-systolic dysfunction is seen on Echo
    • All patients should be given an ACE-inhibitor e.g. lisinopril, ramipril; and a beta-blocker e.g. bisoprolol (unless contraindicated)
      • If the patient is intolerant of an ACEI, an ARB may be an alternative
      • In general, a ‘start low, go slow’ dosing approach for both ACEIs and BBs should be used
  • If symptoms persist, consider adding
    • an ARB e.g. candesartan (with mild-moderate disease)
    • an aldosterone antagonist (e.g. spironolactone) (with moderate-severe disease or with patients with a recent MI)
    • hydralazine in combination with a nitrate (particular in Afro-Caribbean individuals with moderate-severe disease or if intolerant of both ACEI/ARBs)
  • diuretics may be used for alleviation of symptomatic oedema or dyspnoea.  IV diuretics may be required
    • Furosemide is often preferred due to its dual diuretic and vasodilating effect
  • digoxin may be considered an add-on for otherwise refractory disease (it is not, however, to be used as an immediate treatment for acute heart failure)
• Other management
  • For patients with drug-refractory disease who are NYHA class III-IV and have a QRS duration >120ms WITH dyssynchrony on Echo OR QRS>150ms (without), cardiac resynchronisation should be considered
  • Implantable defribillators can also be considered
• Often patients will require intensive input from OT/Physio in Rehabilitation wards/facilities.
• Also, make sure to treat any underlying CVD e.g. hyperlipidaemia with statins; monitor blood pressure closely and adjust drug treatments accordingly; aspirin/clopidogrel will often be required in patients with a history of CHD.

These patients will require follow up, at least six-monthly (a lot more frequently e.g. fortnightly- if there are issues/changes with treatments).  Review BP, FBC, U&Es (renal function), cognitive status, nutritional status, functional capacity etc.