Causes

• Myocardial dysfunction eg IHD, CM

• Volume overload eg AR, MR

• Obstruction eg AS, HCM

• Diastolic dysfunction eg Constriction

• Mechanical problems eg LV aneurysm

• Rhythm disturbance eg A fib

• High output eg anaemia, shunts, thyrotox

Definition

• Cardiac output that is insufficient to meet the needs of the body

Heart failure symptoms• SOBE

• Orthopnoea, PND

• Ankle swelling

• Anorexia, weight loss

• Cold peripheries

• Tiredness

Heart failure signs• Tachycardia, hypotension

• Raised JVP, S3

• May be PSM of MR (or TR)

• Basal crepitations

• Ankle oedema

Not useful to divide into right and left heart failure

ECG, CXR, Echo

• ECG often abnormal– Previous MI, LBBB, Non-specific ST/T abnormalities

– If ECG normal unlikely to be systolic dysfunction

• CXR cardiomegaly– Upper lobe diversion, fluid in horizontal fissure, Kerly

B lines, pleural effusions

• Echocardiography– Confirms / refutes diagnosis of systolic dysfunction

– Can assess diastolic dysfunction

Treatment – Acute heart failure• Sit up

• High dose oxygen

• Intravenous loop diuretic

• Venodilation eg intravenous GTN

• Possibly intravenous diamorphine

• (Aminophylline, venesection)

• Intubation and ventilation

Cardiogenic shock•Severe hypotension

•Poor tissue perfusion - Oliguria, Confusion

•Mortality 80%+

•Inotropes eg Dopamine, Dobutamine

•IABP +/- angioplasty if cardiac ischaemia

Chronic heart failure - Mortality

Treatment – Chronic heart failure

• Salt restriction

• Fluid restriction

• Diuretics– Usually loop diuretics– Occasionally add thiazides

• May lead to excessive diuresis, electrolyte imbalance

• Amiloride, triamtarene may prevent low K

Treatment – vasodilators• Reduce preload / afterload

– ACEI• Reduce morbidity and mortality• Interact with RAAS• Prevent adverse remodelling post MI• May precipitate renal failure• Cough in 10-15% (consider AII blockers)

– Nitrates and hydralazine• Reduce morbidity / mortality but less than ACEI

Treatment - inotropes• Digoxin

– Reduces hospital admissions

– No reduction in mortality

– Stopping may precipitate deterioration

• All other oral positive inotropes to date have caused an increased mortality

Treatment – beta blockers

•Recent studies suggest beta-blockers improve morbidity and mortality

•Similar degree to ACEI and additive

•Possibly via reduction in sympathetic activation

•May precipitate pulmonary oedema

–Start low doses and slowly titrate up

Treatment - spironolactone

• Recently shown to improve mortality in severe heart failure

• Probably via blockage of aldosterone• May precipitate hyperkalaemia and renal failure

Heart failure rule of halves

Diastolic heart failure• Up to a third of patients have clinical heart failure with

normal LV systolic function

• Underlying pathophysiology relates to diastolic dysfunction

• Commonest underlying pathologies

– Normal ageing, Hypertension, Myocardial ischaemia

Mechanisms of diastolic dysfunction

•Impaired ventricular relaxation

–Energy dependent process

–Susceptible to myocardial ischaemia

•Decreased myocardial compliance

–Altered compliance mediated by collagen

–Fibrosis related to activation of RAAS

Doppler patterns of diastolic dysfunction

• Impaired relaxation– Reduced E/A ratio

– Increased EDT

– Increased IVRT

• Restriction– LA pressure increases due to myocardial stiffness

– High peak E wave velocity

– Short EDT

– Very short IVRT

Treatment of diastolic heart failure• Treat underlying cause eg ischaemia

• Impaired relaxation

– Theoretically rate-limiting agents effective

• Beta-blockers, verapamil

• Reduce HR and prolong diastole

• Reduce myocardial oxygen demand

• Lower BP and reduce LVH

•Restriction

–Drugs which reduce fibrosis and lower LA pressure theoretically should be effective

•ACEI, AII blockers, Diuretics

–If LA pressure lowered too much cardiac output significantly worsened

•Can cause significant morbidity