What is heart failure?
Heart failure is state in which heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure.
A pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with requirements of the metabolising tissues.
A clinical syndrome caused by an abnormality of the heart and recognised by a characteristic pattern of haemodynamic, renal, neural and hormonal responses.
Describe the aetiology of heart failure
Ischaemic Heart Disease is the primary cause of Systolic HF (~70%) e.g. previous MI
Other causes of HF:
Dilated cardiomyopathy (non-ischaemic)
- Bugs (viral/bacterial/mycobacteria)
- Pregnancy (peri-partum)
Valvular Heart Disease / Congenital
Restrictive Cardiomyopathy e.g. amyloidosis (deposition in LV wall)
High-output heart failure
Arrhythmias (e.g. if patient doesn’t receive treatment for AF => dilation of ventricles)
Describe the progression of heart failure
NYHA Functional Classification
Class I: no symptomatic limitation of physical activity
- Slight limitation of physical activity
- Ordinary physical activity results in symptoms
- No symptoms at rest
- Marked limitation of physical activity
- Less than ordinary physical activity results in symptoms
- No symptoms at rest
- Inability to carry out any physical activity without symptoms
- May have symptoms at rest
- Discomfort increases with any degree of physical activity.
Heart failure prognosis is worse than most cancers – very severe!
Describe the clinical syndromes in heart failure
in clinical practice, heart failure is often divided into:
Right sided heart failure
Left sided heart failure
Biventricular (congestive) cardiac failure
Systolic heart failure (‘pump failure’)
Diastolic heart failure (failure of relaxation)
IT IS LESS COMMON FOR ANY PART OF THE HEART TO FAIL IN ISOLATION
Draw the Starling Curve in Mild and Gross Heart Failure
Starling’s Law of the Heart: the force developed in a muscle fibre depends on the degree to which the fibre is stretched
What happens in Systolic Dysfunction
: failure of the left ventricle to pump properly
Increased LV capacity (LV dilatation)
Reduced LV cardiac output
Thinning of the myocardial wall
- Fibrosis and necrosis of myocardium
- Activity of matrix proteinases
Mitral valve incompetence (doesn’t close properly => functional mitral regurgitation (structurally normal))
What structural changes would you see in diastolic and systolic heart failure?
Ventricular remodelling after acute infarction
- Expansion of infarct (hours to days)
- Global remodelling (days to months)
Ventricular remodelling in diastolic and systolic heart failure
- Diastolic heart failure: hypertrophied heart
- Systolic heart failure: dilated heart
What does cardiac output depend on?
What is Diastolic Dysfunction
Diastolic Dysfunction (Heart Failure with Normal Ejection Fraction)
20-50% of heart failure patients
- Frequently elderly and female
- Often history of hypertension/diabetes/obesity
Normally LV function but concentric left ventricular hypertrophy
Hospitalisation and mortality similar to systolic HF
Diagnosis is less clear cut
Little clinical outcome study data to guide therapy
Describe Diastolic Dysfunction procedures
Reduced LV compliance
Impaired myocardial relaxation
Impaired diastolic LV filling (but with increased LA and PA pressures)
Unable to compensate by increasing LV EDP (Frank Starling)
Low cardiac output results
Triggers neuro-hormonal activation as per systolic heart failure.
What is preload and afterload?
Preload: end diastolic volume – initial stretching of the cardiac myocytes prior to contraction.
Afterload: pressure that the chambers of the heart have to generate to eject blood – the end load against which the heart contracts to eject blood.
What is meant by Neuro-Hormonal Activation?
Sympathetic Nervous System
Tissue Necrosis Factor - alpha
Describe the up-regulation of the Sympathetic Nervous System in HF
Baroreceptor-mediated response (baroreceptors innervated by glossopharyngeal and vagal afferents) to increase heart rate
Early compensatory mechanism to improve CO:
- Cardiac contractility
- Arterial and venous vasoconstriction
However long-term deleterious effects
B-adrenergic receptors are down-regulated/uncoupled
- Induces cardiac hypertrophy/myocyte apoptosis and necrosis via alpha-receptors (direct cardiotoxicity)
- Induce up-regulation of the RAAS
Reduction in heart rate variability (reduced parasympathetic nervous system and increased sympathetic nervous system) (vicious cycle)
The Renin-Angiotensin-Aldosterone System (RAAS)
RAAS is commonly activated in HF:
- Reduced renal blood flow
- SNS induction of renin from macula densa
Renin converts Angiotensinogen into Angiotensin I.
Angiotensin I is converted into Angiotensin II by Angiotensin Converting Enzyme (lungs and vasculature)
What are the effects of elevated AT2?
Promotes LVH (left ventricle hypertrophy) and myocyte dysfunction
Promotes aldosterone release
Promotes Na+/H2O release
Stimulates thirst by central action?
What are renal effects in HF?
GFR is maintained in early HF by haemodynamic changes at the glomerulus.
Increased Na+/H2O retention due to neuro-hormonal activation.
However in severe HF, renal blood flow falls (reduced renal perfusion) leading to reduced GFR (via vasoconstriction) and a subsequent rise in serum urea and creatinine.
This can be exacerbated by treatment inhibiting the actions of Angiotensin II
What are the symptoms of left heart failure
Exertional dyspnoea (at rest = severe) (struggle to eat)
Orthopnoea (number of pillows)
Paroxysmal nocturnal dyspnoea (opening windows)
Ankle swelling (often minimised) (due to RAAS activation => Na+ + H2O retention)
What are the signs of heart failure?
Blood pressure: depends on aetiology
Cardiomegaly (displaced apex beat, may be sustained)
3rd or 4th heart sound (gallop murmur)
Functional murmur of mitral regurgitation (systolic blowing murmur)
Basal pulmonary crackles
Peripheral oedema (compared to RHF)
Peripheral oedema and basal pulmonary crackles due to fluid overloading but in LHF, JVP is unlikely to be raised.
Describe the aetiology of right heart failure?
Chronic Lung Disease
Pulmonary embolism/pulmonary hypertension
Pulmonary/tricuspid valvular disease
Left-to-right shunts (ASD/VSD)
Isolated right ventricular cardiomyopathy
The most frequent cause is secondary to left heart failure
What are the symptoms/signs of 'pure' right heart failrue?
(Relate to distension and fluid accumulation in areas drained by the systemic veins) (congestion)
Fatigue, dyspnoea, anorexia, nausea
Tender, smooth hepatic enlargement
Dependent pitting oedema
How would you investigate heart failure?
- Full blood count (look at Hb to see if anaemia is exacerbating HF)
- Renal function and electrolytes (is there renal function impairment or concurrent renal disease? Any drug contraindications?)
- BNP (brain natural peptide)
ECG (left bundle branch block is often associated with dilated cardiomyopathy
CXR – to detect cardiomegaly
- Kerley lines are a sign seen on chest radiographs with interstitial pulmonary oedema. They are thin linear pulmonary opacities caused by fluid or cellular infiltration into the interstitium of the lungs.
Echocardiography – gold-standard
Describe the management of heart failure principles. What are the aims of pharmacological therapy?
Correct underlying cause (is there underlying ischaemia? Consider stenting, angiography)
- Symptomatic improvement
- Delay progression of heart failure
- Reduce mortality
Treat complications/associated conditions/cardiovascular risk factors e.g. arrhythmia
Describe what lifestyle modification would involve
Increase aerobic exercise
Decrease blood pressure
What would pharmalogical therapy involve?
Diuretics (loop) (initial therapy furosemide)
Beta-blocker (add-on therapy to ACEi/ARB)
Spironolactone (add-on therapy to ACEi/ARB) – can especially be beneficial in isolated RHF so consider early on
(Digoxin) (Maybe suitable for AF? Uncertain how advantageous)
(Inotropes – acute setting)
Phosphodiesterase inhibitors – acute setting
Aniarrhythmics (if rhythm disturbance)
What would cardiac surgery involve?
Mechanical assist devices
- E.g. valve surgery
- Revascularisation (PCI, CABG)
Biventricular pacing (to allow synchronous pumping of the heart e.g. in LBBB – can significantly improve cardiac output)
Implantable defibrillators (if risk of ventricular fibrillation)
What do you need to remember about ACEi/ARBs and hyperglycaemia in acute HF?
ACE inhibitors inhibit Angiotensin Converting Enzyme breaking down bradykinin. Bradykinin leads to vasodilation as it increases the production of Nitric Oxide. An accumulation of bradykinin in the lungs leads to a cough.
Angiotensin Receptor blockers block AT1 receptors leading to ATII binding to AT2 receptors. This has a beneficial effect as it increases the production of nitric oxide leading to vasodilation.
Patients with acute HF: hyperglycaemia has a significant impact on mortality => require aggressive treatment