how to diagnose heart failure - pathkids.com
TRANSCRIPT
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How to Diagnose
Heart Failure
Patrick J Gallagher
12th November 2014
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Sudden Cardiac Death
Davies’ Criteria
1. Acute coronary event ± infarction
2. Coronary narrowing + healed infarction
3. Coronary narrowing but no infarction
4. Heart failure (without coronary narrowing)
5. Structurally normal heart
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History and Epidemiology
• Descriptions of heart failure from
ancient Egypt, Greece and India
• The Romans may have used foxglove
(digitalis). William Withering saw the
benefical effects in 1785
• Blood letting was a popular treatment
for many symptoms during the 18th
and 19th
Centuries
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Edward Jenner Museum
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History and Epidemiology
• Cardiac failure is increasing in
prevalence and is one of the most
important serious illnesses in practice
• Prevalence is between 3 and 20 per
1000 population. An important cause
of death in many 3rd
world countries
• Median survival is less than 3 years,
much worse than cancer of the large
bowel or breast
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Cardiac Failure in Different
Population Groups
• Coronary heart disease and
hypertension are the leading causes in
the West
• Hypertension is an important cause of
cardiac failure in Afro-Caribbeans
• A combination of coronary heart
disease and diabetes is important in
Asians
• Valve disease is especially important
in India and parts of Central Africa
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Pathophysiology of Heart Faiure
Heart failure is a multisystem disorder
characterised by abnormalities in
cardiac and skeletal muscle and renal
function. There is stimulation of the
sympathetic nervous system,
activation of the renin-angiotensin-
aldosterone system and other
neurohormonal changes
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Pathophysiological Changes
• Baroreceptors sense arterial
underfilling
• Activation of the renin-angiotensin-
aldosterone system stimulates
vasoconstriction and sodium
retention. Blood volume increases by
up to 25%
• Aldosterone causes endothelial and LV
dysfunction and ventricular fibrosis
• Sympathetic stimulation increases
heart rate and causes further
vasoconstriction
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Pathophysiological Changes
• Anti-diuretic hormone (ADH)
concentrations are increased. ADH
causes further sodium and water
retention by counteracting the normal
“waterproofing” of the distal tubule.
Hyponatraemia.
• Atrial stretch causes increased
secretion of natriuetic peptide
hormones (ANP and BNP). These
promote sodium secretion. Broken
down by endopeptidases, such as
naprilysin
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Why is it so difficult to diagnose
Heart Failure at Autopsy
• Details of signs, symptoms,
medications and lab results may not
be in the GP fax
• BNP estimations, CXR/CT and ECHO
reports may not be available
• In treated patients the pathological
changes may not be present
• It is difficult to accept that sudden
death is a feature of early disease
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Arrhythmias and Sudden Death
in Heart Failure• “Patients with heart failure commonly
die suddenly”
• Generally the worse the symptoms and
the lower the EF the greater the risk of
SD
• 15% annual incidence SD with EF 9-
20%, 6% with EF 31-40%
• AF is commoner in older patients, they
have lower EFs and higher risk of SD
Cleland et al Heart Failure Reviews 7;2002:299
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Cardiac failure at Autopsy
Pulmonary Oedema
• Mechanism of agonal pulmonary
oedema is unknown
• A study of nearly 1000 cardiac deaths
showed no relation between cause of
cardiac death and lung weight
• Head injury and drug overdoses are
causes of pulmonary oedema
• Chronic uraemia is rare in our PM
population
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Cardiac Failure at Autopsy
Effusions and Oedema
• Bilateral pleural effusions provide
strong evidence of chronic heart
failure
• Are also seen in combination with
ascites in liver failure
• Assess lower limb oedema carefully,
sensitive not specific for HF
• Look for venous disease, estimate the
degree of induration, look for venous
ulceration
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Careful Grading of Hepatic Congestion is Important
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Diastolic Heart Failure
HFpEF• Most patients with heart failure have
echo evidence of poor ventricular
contraction
• Some have normal LV function. Is the
problem poor diastolic filling?
• The syndrome is more or less defined
physiologically but not pathologically
• Look for evidence of heart failure in
patients with small hearts,
hypertrophied ventricles, small
cavities but no other causes of heart
failure
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Cardiac Muscle Pathology
• Marked variation in heart weight, up to
~ 600g, but can be in the normal
range
• Many cases have no scars and the
muscle itself appears entirely normal
• Histology may demonstrate an
increase in interstitial fibrous tissue
• After SADS Idiopathic LV hypertrophy
with or without fibrosis is the
commonest cause of sudden
unexplained cardiac death
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Normal Myocardium
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Unexplained Heart Failure
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Diabetic Small Vessel Disease ?
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Non-cardiac abnormalities in
chronic heart failure
• Fatigue and malaise are disabling
symptoms in heart failure. Muscle bulk
is lost and there may be structural
abnormalities in muscle
• Many patients are anaemic
• In the majority of patients renal
impairment is the result of the poor
cardiac function (“pre renal renal
failure”)
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Ischaemic Heart Disease
• Many patients with clear evidence of
healed infarction do not have a critical
coronary narrowing
• Critical narrowings may have been
organised and coronary arteries may
dilate as part of remodelling
• The appearance of the epicardial
coronary arteries is no guide to the
micro circulation
• Without histology you can miss
fibrosis
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Hypertension
• Although Hospital and GP records are
more and more accessible many
patients do not have a documented BP
• There is no pattern of LVH that is
diagnostic of hypertension
• Don’t confuse ageing kidneys with
hypertensive or end stage renal
disease
• Think very carefully before diagnosing
hypertensive heart disease
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End Stage Kidneys
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Valvular Disease
• Clinical records are seldom helpful,
murmurs vary and 3rd
and 4th
heart
sounds rarely described. Even a
consistent BP reading may be absent
• Echo report is invaluable
• Some degenerative change in all
elderly patients
• Some murmurs have no structural
basis
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Heart sounds
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Mitral Incompetence
• Probably the commonest significant valvular
abnormality
• It is often difficult to define a cause at post
mortem examination
• In most cases there are no structural
changes in the valve leaflets
• Limited ventricular dilatation or ischaemic
fibrosis may impair mitral valve function
• An important cause of heart failure
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Mitral Valve Degeneration
• A common finding in elderly patients
• Some cases have marked valve
thickening and prolapse. Variable
histological changes
• Prolapse is associated with a mid
systolic click and late systolic murmur
• Results of mitral valve repair are
excellent
• A rare cause of unexpected sudden
death
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Mitral valve prolapse
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Mucoid Degeneration
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Calcification MV Annulus
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Papillary muscle rupture
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Mitral Stenosis
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Mitral Stenosis
• A small number of cases in white
British patients with previous
rheumatic fever
• No progress in understanding of
pathogenesis over 40 years
• Symptoms develop when mitral valve
area reduced to 1 cm2
• Significant mortality associated with
MVR. Balloon valvuloplasty possible
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Mitral stenosis with incompetence
Atrial dilatation
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Atrial Fibrillation
• Suspect AF when there is a history of
digitalis or amiodarone treatment
• There is no established method of
estimating ventricular or atrial size
• Look carefully at the atrial appendages
• Don’t forget to examine the thyroid.
Very few thyroids in elderly patients
are completely normal
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Normal aortic valve M66
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Aortic Stenosis
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Aortic Stenosis
• An important cause of sudden unexpected
death.
• Risk factors similar to those for atheroma.
Emerging evidence that there is low grade
chronic inflammation in the cusps
• Previous rheumatic fever is now a rare cause
of aortic stenosis.
• Gradient is related to valve area, e.g.
6mm @ 2cm2, 26 mm @ 1cm
2 but 105mm @
0.5 cm2
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Diagnosis
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Infective Endocarditis
• Native valve
• Prosthetic valve
• Drug abuse
• Hospital acquired infections
• After interventions, e.g.
haemodialysis, pacemakers etc
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Infective Endocarditis
• The full range of signs and symptoms
described in classical texts are now
rarely present
• For various reasons about 15% of
genuine cases with echo changes are
culture negative
• S. aureus is now a common causative
organism
• Cases that do not respond rapidly to
antibiotic therapy are considered for
valve replacement
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Bacteraemia & Septicaemia
• Bacteria can enter the blood stream
from the mouth, gastrointestinal tract,
the skin and any source of infection
• Normally rapidly opsonised and
phagocytosed and cleared by the
spleen
• In septicaemia larger numbers of
bacteria set up a chain of reactions
which generate cytokines and may
cause shock
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Septic (Endotoxic) Shock
• LPS-LPB complexes bind to specific
pattern recognition receptors on the
surface of monocytes/macrophages.
This causes cytokine secretion,
especially tumour necrosis factor α(TNFα)
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Septic (Endotoxic) Shock
• TNF-α stimulates release of other
cytokine molecules, such as IL-1 and
IL-6 and may directly injure tissues
• TNF-α also increases the expression of
adhesion molecules (e.g.ICAMs) which
increase leucocyte adhesion to
endothelium
• Tissue factor release promotes
coagulation
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Pathophysiology of IE
• In theory opsoninisation and
phagocytosis should kill Gram positive
organisms and lead to resolution
• In IE bacteria grow on the surface of
valves, capped by a layer of fibrin.
Easy access to nutrients, protected
from phagocytes
• In this privileged site organisms
proliferate slowly and form masses
called vegetations
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Infective endocarditis
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Changing Patterns of IE
• Although the overall incidence may be
falling it is rising in elderly patients
• Improved dental hygiene has reduced
streptococcal endocarditis
• Staphylococci are now the leading
cause. Especially associated with
haemodialysis, diabetes and iv drugs
• The advantages of intravascular
devices must be weighed against the
risk of IE
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Complications of Valve
Replacement
• Perioperative ventricular rupture
• Infective endocarditis
• Valvular thrombosis
• Periprosthetic leak
• Structural failure
• Calcification of homografts
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Carpentier Ring
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Prosthetic valve endocarditis
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Acute prosthetic valve thrombosis
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Organising thrombosis of prosthetic valve
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Periprosthetic leak
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Structural failure of bioprosthetic valves
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Summary
• Hepatic congestion, pleural effusions,
LV dilatation & hypertrophy, limb
oedema
• Overlap between CCF and DCM,
especially in the elderly
• Aortic stenosis is an undoubted cause
of sudden death. Look out for
bicuspids and refer relatives to Drs
Curtis/Stuart
• Ischaemic mitral incompetence is
difficult to assess at PM